__Pelvic_Floor_Re_education__Principles_and_Practice__Second_Edition

Pelvic Floor Re-education

Kaven Baessler, Bernhard Schussler, Kathryn L. Burgio, Kate H.Moore, Peggy A. Norton, and Stuart L. Stanton (Eds.) Pelvic Floor Re-education Principles and Practice Second Edition ~ Springer

Kaven Baessler, MD Bernhard Schussler, MD, PhD Consultant Gynaecologist Professor of Obstetrics and Gynaecology Department of Gynaecology Neue Frauenklinik Charite University Hospital Kantonsspital Luzern Berlin, Germany Luzern, Switzerland Kate H. Moore, MBBS, MD, FRCOG, Kathryn 1. Burgio, PhD Professor of Medicine FRANZCOG, CU Division of Gerontology, Geriatrics Associate Professor Department of Urogynaecology and Palliative Care University of New South Wales Department of Medicine St George Hospital University of Alabama at Birmingham Sydney, NSW, Australia Birmingham, AL, USA Stuart 1. Stanton, FRCS, FRCOG, and FRANZCOG(Hon) Associate Director for Professor of Pelvic Floor Reconstruction and Geriatric Research, Education, and Urogynaecology Clinical Center Portland Hospital Birmingham Veterans Affairs Medical Center London, UK Birmingham, AL, USA Peggy A. Norton, MD Professor Chief of Urogynecology and Reconstructive Pelvic Surgery Department of Obstetrics and Gynecology University of Utah School of Medicine Salt Lake City, UT, USA Library of Congress Control Number : 2006926873 British Library Cataloguing in Publication Data Pelvic floor re-education : principles and practice. - 2nd ed. 1. Pelvic floor 2. Urinary incontinence - Exercise therapy I. Baessler, K. 616.6'2 ISBN-13: 9781852339685 ISBN: 978-1-85233-968-5 2nd edition e-ISBN: 978-1-84628-505-9 Printed on acid-free paper DOl: 10.1007/978-1-84628-505-9 ISBN: 3-540-19860-1/3-540-76145-4 1st edition © Springer-Verlag London Limited 2008 First published 1994; Second edition 2008 The software disk accompanying this book and all material contained on it is supplied without any war- ranty of any kind. The publisher accepts no liability for personal injury incurred through use or misuse of the disk . Apart from any fair dealing for the purposes of resear ch or private study, or crit icism or review, as permitted under the Copyright, Designs and Patents Act 1988, this publication may only be reproduced, stored or trans- mitted, in any form or by any means, with the prior permission in writing of the publishers, or in the case of reprographic reproduction in accordance with the terms oflicences issued by the Copyright Licensing Agency. Enquiries concerning reproduction outside those terms should be sent to the publishers. The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of a spe- cific statement, that such names are exempt from the relevant laws and regulations and therefore free for general use. Product liability: The publisher can give no guarantee for information about drug dosage and applicat ion thereofcontained in this book . In every individual case the respective user must check its accuracy by consult- ing other pharmaceutical literature. 98765 432 1 springer.com

Preface This book is designed to provide a clinically useful overview of our field - Urogynecol- ogy and Reconstructive Pelvic Surgery. Each chapter is meant to give a thorough yet concise amount of information. We assembled a world-class group of authors and asked each of them to focus on the information that they use in practice every day. This text is appropriate for general gynecologists, physiotherapists, obstetrician- gynecologists, urologists, family practice and internal medicine physicians, nurse practitioners, physician assistants, and any other practitioners who regularly find themselves caring for women with pelvic floor dysfunction. Kaven Baessler Bernhard Schiissler Kathryn L. Burgio Kate H. Moore Peggy A. Norton Stuart L. Stanton v

Contents Preface v Contributors Xl Part I Function and Dysfunction of the Pelvic Floor and Viscera 3 1.1 Functional Anatomy of the Pelvic Floor and Lower Urinary Tract 22 Daniele Perucchini and fohn O.L. DeLancey 36 49 1.2 Neural Control of Pelvic Floor Muscles 62 David B. Yodui ek 71 75 1.3 The Effects of Pregnancy and Childbirth on the Pelvic Floor 83 Kaven Baessler and Bernhard Schussler 91 1.4 Muscle Function and Ageing 105 Brenda Russell and Linda Brubaker vii 1.5 Urinary Incontinence and Voiding Dysfunction Annette Kuhn and Bernhard Schussler 1.6 Pelvic Organ Prolapse Peggy A. Norton 1.7 Anal Incontinence, Constipation, and Obstructed Defecation Abdul H. Sultan and A. Muti Abulaffi 1.8 Overactive Pelvic Floor Muscles and Related Pain Wendy F. Bower Part II Evaluation of the Pelvic Floor 2.1 Clinical Evaluat ion of the Pelvic Floor Muscles Diane K. Newman and fo Laycock 2.2 Examination of Patients with Pelvic Organ Prolapse Ursula M. Peschers

viii Contents 109 2.3 Urodynamics 120 Ursula M. Peschers 124 135 2.4 Applying Urodynamic Findings to Clinical Practice 144 Christopher K. Payne 155 162 2.5 Anorectal Physiology David Z. Lubowski and Michael L. Kennedy 2.6 Ultrasound Imaging Kaven Baessler and Heinz Kblbl 2.7 Magnetic Resonance Imaging Thomas Treumann, RalfTunn, and BernhardSchussler 2.8 Electrophysiology Clare J. Fowler and David B. Yodusek 2.9 Outcome Measures in Pelvic Floor Rehabilitation Kate H. Moore and Emmanuel Karantanis Part III Techniques of Pelvic Floor Rehabilitation and Muscle Training 3.1 Concepts of Neuromuscular Rehabilitation and Pelvic Floor 177 Muscle Training [a Laycock 3.2 Exercise, Feedback, and Biofeedback 184 Pauline E. Chiarelli and Kate H. Moore 3.3 Electrical Stimulation 190 Wendy F. Bower 3.4 Extracorporeal Magnetic Stimulation 196 Alastair R. Morris and Kate H. Moore 3.5 Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201 Ingrid Nygaard and Peggy A. Norton 3.6 Alternative Methods to Pelvic Floor Muscle Awareness 208 and Training\" Kaven Baessler and Barbara E. Bell * The authors gratefully acknowledge theassistance ofErna Alig in thepreparation ofthis chapter.

Contents ix Part IV Treatment: Condition-Specific Assessment and Approaches 215 221 4.1 Behavioral Treatment Kathryn L. Burgio 228 235 4.2 Stress Urinary Incontinence 242 246 Jo Laycock 253 259 4.3 Evidence for the Effectiveness of Pelvic Floor Muscle 267 Training in the Treatment and Antenatal Prevent ion of 271 Female Urinary Incontinence E. Jean c. Hay-Smith and Kate H. Moore 4.4 Postpartum Management of the Pelvic Floor Pauline E. Chiarelli 4.5 Role of a Perineal Clinic Ranee Thakar 4.6 Overactive bladder Kathryn L. Burgio, Dudley Robinson, and Linda Cardozo 4.7 Sexual Dysfunction and the Overactive Pelvic Floor Wendy F. Bower 4.8 Anal Incontinence and Evacuation Difficulties Christine Norton 4.9 Incontinence During Sports and Fitness Activities Alain P. Bourcier 4.10 Pelvic Organ Prolapse - Pessary Treatment Jane A. Schulz and Elena Kwon Part V What to Do if Physiotherapy Fails? 5.1 Stress Urinary Incontinence: Choice of Surgery 281 Stuart L. Stanton 5.2 Genital Prolapse: Surgery for Failed Conservative Treatment 285 Stuart L. Stanton 5.3 The Anal Sphincter 289 Klaus E. Matzel, Manuel Besendbrfer, and Stefanie Kuschel Index..... .. . . . .. . . . .. ..... . . .. .... .. .... ... .. . ............ . .. ... . . . . . 293

Contributors A. Muti Abulaffi, MS, FRCS Linda Brubaker, MD, MS, FACOG, FACS Colorectal Unit Department of Obstetrics and Gynecology Mayday University Hospital Female Pelvic Medicine and Reconstructive Croydon, UK Surgery Kaven Baessler, MD Loyola University Medical Center Department of Gynaecology Maywood, IL, USA Charite University Hospital Berlin, Germany Kathryn L. Burgio, PhD Division of Gerontology, Geriatrics and Palliative Barbara E. Bell, BSc, BA Pelvic Power Care Chemmart Pharmacy Department of Medicine Acacia Ridge, QLD, Australia University of Alabama at Birmingham Birmingham, AL, USA Manuel Besendorfer, MD and Geriatric Research, Department of Surgery University Hospital Erlangen Education, and Clinical Center Erlangen, Germany Birmingham VA Medical Center Birmingham, AL, USA Alain P. Bourder, PT Pelvic Floor Rehabilitation Services Linda Cardozo, MD, FRCOG Department of Urology Department of Urogynaecology Tenon Hospital Kings College Hospital Paris, France London, UK Wendy F. Bower, phD Pauline E. Chiarelli, PhD Department of Surgery Discipline of Physiotherapy Division of Pediatric Surgery and Pedriatric School of Health Sciences University of Newcastle Urology Callaghan, NSW, Australia The Chinese University of Hong Kong Prince of Wales Hospital John O.L. DeLancey, MD Hong Kong, China Department of Obstetrics and Gynecology Women's Hospital Ann Arbor, MI, USA xi

xii Contributors Clare J. Fowler, FRCP Klaus E. Matzel, MD, PhD Department of Uro-Neurology Section of Coloproctology Institute of Neurology Department of Surgery London, UK University Hospital Erlangen Erlangen, Germany E. Jean C. Hay-Smith, PhD, MSc Rehabilitation Teaching and Research Unit Kate H. Moore, MBBS,MD, FRCOG, Department of Medicine FRANZCOG, CU Wellington School of Medicine and Health Department of Urogynaecology Sciences University of New South Wales University of Otago St George Hospital Wellington, New Zealand Sydney, NSW, Australia Emmanuel Karantanis, BMed, MBBS, UNSW, Alastair R. Morris, MBChB, MRCOG, FRANZCOG FRANZCOG, FRCSEd, MD St George Hospital Department of Obstetrics and Gynaecology Sydney, NSW, Australia Royal North Shore Hospital Sydney, NSW, Australia Michael 1. Kennedy, BSc Colorectal Research Fellow Diane K. Newman, RNC, MSN, CRNP, FAAN St George Hospital Medical Centre Penn Center for Continence and Pelvic Health Sydney, NSW, Australia Division of Urology University of Pennsylvania Health System Heinz Kolbl, MD Philadelphia, PA, USA Gynecology and Obstetrics Johannes-Gutenberg Universitat Christine Norton, PhD, MA, RN Mainz, Germany Burdett Institute of Gastrointestinal Nursing King 's College London Annette Kuhn, MD St Mark's Hospital Department of Urogynecology Harrow, UK Frauenklinik Inselspital Bern, Switzerland Peggy A. Norton, MD Urogynecology and Reconstructive Pelvic Stefanie Kuschel, MD Department of Obstetrics and Gynecology Surgery Kantonsspital Luzern Department of Obstetrics and Gynecology Luzern, Switzerland University of Utah School of Medicine Salt Lake City, UT, USA Elena Kwon, BSc Faculty of Medicine Ingrid Nygaard, MD University of Alberta Department of Urogynecology Edmonton, AB, Canada University of Utah Health Science Center Salt Lake City, UT, USA Jo Laycock, PhD, FCSP The Culgaith Clinic Christopher K. Payne, MD, FACS Penrith, UK Section of Female Urology and NeuroUrology Stanford University School of Medicine David Z. Lubowski, MD, FRACS Stanford, CA, USA Department of Colorectal Surgery St George Hospital Medical Centre Daniele Perucchini, MD Kogarah, NSW, Australia Department of Obstetrics and Gynecology University Hospital Ziirich and Praxis am Stadelhoferplatz Ziirich, Switzerland

Contributors xiii Ursula M. Peschers, MD Stuart L. Stanton, FRCS,FRCOG, FRANZCOG Department of Obstetrics and Gynecology (Hon) Frauenklinik Dachau, Germany Pelvic Floor Reconstruction and Urogynaecology Portland Hospital Dudley Robinson, MBBS, MRCOG London , UK Department of Urogynaecology Kings College Hospital Abdul H. Sultan, MBChB, MD, FRCOG London, UK Department of Obstetrics and Gynaecology Mayday University Hospital Brenda Russell, PhD Croydon, UK Department of Physiology and Biophysics The University of Illinois at Chicago Ranee Thakar, MD, MRCOG Chicago, IL, USA Department of Obstetrics and Gynaecology Mayday University Hospital Jane A. Schulz, MD, FRCSC Croydon, UK Urogynecology Unit Department of Obstetrics and Gynecology Thomas Treumann, MD Royal Alexandra Hospital Institute of Radiology Univers ity of Alberta Kantonsspital Luzern Community Services Centre Luzern, Switzerland Edmonton, AB, Canada Ralf Tunn, MD Bernhard Schussler, MD, PhD German Pelvic Floor Center, Urogynecology Neue Frauenklinik St Hedwig Hospitals Kantonsspital Luzern Berlin , Germany Luzern, Switzerland David B. Vodusek, MD, PhD Video Material on the DVD Division of Neurology University Medical Centre Stefanie Kuschel, MD Ljubljana, Slovenia Department of Obstetrics and Gynecology Kantonsspital Luzern Luzern, Switzerland

Part I Function and Dysfunction of the Pelvic Floor and Viscera

1.1 Functional Anatomy of the Pelvic Floor and Lower Urinary Tract Daniele Perucchini and John 0.1. DeLancey Key Message pelvic container and includes all of the structures that lie between the pelvic peritoneum and the Pelvic floor rehabilitation is dependent on a vulvar skin (Fig. 1.1.1). meticulous insight into relevant anatomy. There- fore, this chapter describes not only the anatomy Pelvic floor disorders are common, affecting of the organs and muscles involved but also their one in nine women.' They include pelvic organ topography and innervation. Predominantly its prolapse, urinary incontinence, and anal incon - focus is on functional anatomy. Besides other tinence. These are debilitating conditions that issues, the following questions, which are neces- not only lead to medical problems and costs but sary for understanding pelvic floor function, are are also associated with embarrassment that can extensively discussed: lead to isolation, loss of independence, and dimi- nished quality of life. • How is the pelvic floor muscle (PFM) able to empower the urethral closure mechanism? The levator ani muscles are the primary source of support for the pelvic organs . These muscles • What are the anatomical deficiencies related close off the pelvic floor, allowing structures to the prevention of successful pelvic floor that lie above them to rest on the upper surface re-education? of the muscle. This closure is usually remarkably effective; however, because of injuries and dete- • How are the pelvic organs kept in place? rioration of the muscles, as well as of the nerves • What is the anatomical deficit when stress and connective tissue that support and control normal funct ion, urinary incontinence, fecal urinary incontinence (SUI) or prolapse occurs? incontinence, and pelvic organ prolapse can • What is the mechanism of the anal sphincter result. unit? Female incontinence is strongly associated with pregnancy, childbirth, and ageing. However, Introduction there is universal consensus that the pathophy- siology of urinary incontinence and pelvic The bony pelvis lies in the middle of the human organ prolapse is multifactorial and incompletely body. It supports the spinal column, which understood. Incompetence of the sphincter attaches to it posteriorly, and provides the points mechanism, weakness of the muscles that support of articulation for the femur and the lower the urethra and bladder neck, overactive detru- extremities. It cradles the abdominopelvic organs sor muscle, neurological disorders, injury during that rest above and within it; however, because childbirth or other trauma, age-related changes the bony pelvis is only a hollow ring, its contents in structural integrity, nervous control, hormone would plummet to the ground unless it had a balance, and systemic disease have all been bottom. The \"pelvic floor\" is the bottom of this implicated as causative agents. 3

4 D. Perucchini and J.O.L. Delancey lead to the loss of continence early in life, even if an individual was born with a \"good\" continence mechanism (black line). Little is known about the individual risk factors for incontinence and pro- lapse; therefore, it is difficult to identify women who are at risk. Nulliparous women without known damage to the pelvic floor may also leak urine. In a series of studies, approximately 30% of young, nullipa- rous, healthy, athletic women experienced prob- lems with incontinence. The sports producing the highest percentage of incontinence occur- rence were gymnastics (67%) and basketball (66%).4 This suggests that there is a continence threshold that when exceeded can result in urine loss, even in the absence of known risk factors for incontinence. FIGURE 1.1.1. Overview of pelvic anatomy. The pelvic floor ~ extends between thetwo red areas (peritoneum and levator ani -§ Event A If (delivery) Event B muscle). re=rectum, ut=uterus, bl =bladder, sy =pubic sym- (delivery) physis, va =vagina, and la =levator ani muscles. <co:Il A consensus also exists that the continence <c:Il mechanism deteriorates over time . The preva- lence of prolapse increases with age,' and vaginal o'Eo birth confers a 4-11 fold increase in the risk of developing pelvic organ prolapse that increases '0 with higher parity.' The deterioration of pelvic floor function may be acute, as with vaginal E delivery. There may be recovery after that acute injury until another acute injury occurs, or there en:::l may be a gradual decline in function, especially with age.' As graphically depicted in Figure 1.1.2, Increasing Age despite a repeatedly damaged continence mecha- nism, a patient is able to retain continence and FIGURE 1.1.2. Deterioration of pelvic floor function over a life- compensate for the damage (blue line). Compen- time. Continence is achieved ifthesum ofall continence factors sation is possible because the damage to the remains over the (imaginary) continence threshold (blue area). pelvic floor and the continence control system Events Aand B(pregnancy/delivery) and ageing contribute tothe remain above the continence threshold. deterioration ofthecontinence mechanism (pelvic floor) .Various scenarios are possible: An individual may begin with far less reserve • Blue line: Despite the fact thatthe continence mechanism is (red line), and although the number and magni- tude of the insults she suffers over time are no repeatedly damaged, a patient is able toremain continent and greater than in a women who remains continent, compensate thedamage. her initial low reserve level leads to incontinence • Red line: An individual may start with far less reserve initially, over her lifespan. even though the number and magnitude of the insults she suffers over time are no greater than in women who remain Pregnancy and devastating damage to the continent. She has less reserve and, therefore, becomes incon- pelvic floor because of a difficult delivery can tinent during her life. • Black line: Devastating damage as consequence of an acute insult (event A) can lead toloss ofcontinence early in life, even ifanindividual was born with good continence factors.

1.1. Functional Anatomy ofthe Pelvic Floor and lower Urinary Tract 5 This chapter addresses the functional anatomy tion of the detrusor muscles' relaxation is released of the pelvic floor in women and, specifically, and a reflex voiding contraction is initiated. This focuses on how the pelvic organs are supported is often referred to as the emptying phase, during by the surrounding muscle and fasciae. This which the tone of the urethral sphincter is relaxed chapter also addresses how pelvic visceral func- and bladder detrusor muscles contract in a spiral tion relates to the clinical conditions of urinary fashion. incontinence and pelvic organ prolapse. The Bladder Neck Anatomy ofthe Lower Urinary Tract The term \"bladder neck\" denotes the area at the base of the bladder where the urethral lumen Clinicians have traditionally divided the lower passes through the thickened musculature of the urinary tract into the bladder and urethra (Fig. bladder base (Fig. 1.1.3 A). It is a region where the 1.1.1). At the junction of these two continuous, yet detrusor musculature surrounds the trigonal discrete, structures lies the vesical neck . ring and the urethral meatus', therefore, it is sometimes considered part of the bladder mus- The Bladder culature, but it also contains the urethral lumen. The bladder neck has come to be considered sep - The bladder lies in the anterior (ventral) part of arately from the bladder and urethra because of the pelvic cavity (Fig. 1.1.1). The proportion of the its unique functional characteristics. The bladder cavity that it occupies is dependent on the volume neck plays an important role in the initiation of of fluid contained within the vesical lumen. micturition. Its opening, coupled with the relax- Vesical filling results in direct contact between ation of the urethra, is required during bladder the bladder and the anterior abdominal wall emptying. Urine entering into the proximal above the pubic symphysis. The bladder is com- urethra through an open bladder neck can also posed of an epithelium surrounded by layers of contribute to the sensation of urgency and facili- smooth muscle . The urothelium is much more tate detrusor overactivity. In patients with SUI, than a classical barrier that separates urine from increased bladder neck mobility is often present. extracellular fluid. It is also an active absorptive Specifically, damage to this area results in its epithelium and secretory tissue. The urothelium remaining open while at rest .\" has specialized cell-surface proteins and ion pumps, plus proteglycans and glycoproteins, all Innervation ofthe Bladder of which function together to maintain the imper- meability of the membrane.v\" These same mech- The bladder receives sympathetic innervation anisms also provide an active defense against from the superior hypogastric plexus via hypo- bacterial colonization. gastric nerves into the inferior hypogastric plexus. Postganglionic fibers primarily innervate Bladder Function the bladder base and urethra. At the level of the inferior hypogastric plexus, contributions from The primary function of the bladder is the storage the S2-S4 preganglionic fibers join the sympa- of urine. The secondary function is the evacua- thetic nerves to form the pelvic plexus. These tion of urine (voiding). As a muscle, the detrusor parasympathetic fibers lead to ganglia in the wall must accommodate both processes using a of the bladder, where the postganglionic fibers \"storage phase\" and an \"emptying phase.\" During innervate the detrusor muscle. Afferent fibers the storage phase, the muscular layers relax to toward the pelvic plexus and central nervous facilitate urine so that increasing physiologic system travel with both the sympathetic and volumes may be stored without any appreciable parasympathetic fibers. Overactivity of the detru- increase in intravesical pressure. When the sor muscle is attributed to increased activity bladder reaches its physiological capacity or when of the parasympathetic components, and anti- a woman voluntarily voids, cerebral tonic inhibi- cholinergic agents have become a mainstay of therapy.

6 D. Perucchini and J.O.L. Delancey A.\". 1.1.3 A). The urethra lies on a supportive layer that is composed of the endopelvic fascia and the anterior vaginal wall (Fig. 1.1.4). This layer gains structural stability through its lateral attachment to the arcus tendineus fascia pelvis (ATFP) and arcus tendineus levator ani (ATLA) muscles' :\" and through connections to the pelvic bones by the pubourethral ligaments, which contain dense connective tissue and smooth muscle.\" The integrity of all of these connections is important for the transmission of PFM contraction to the closure function of the urethra. The female ure- thral wall contains concentric layers of muscle, connective tissue, and vasculature that contrib- ute to urethral closure and are relevant for under- standing lower urinary tract dysfunction. \" B FIGURE 1.1.3. A. Normal urethral anatomy of a nulliparous FIGURE 1.1.4. Midurethral cross-section with the levator ani woman.The outermost layer (red)is composed ofstriated muscle muscle visible on both sides ofthe urethra. The outermost layer thathas three components:thesphincter urethra,thecompressor ofthe urethra iscomposed ofstriated muscle (STM). The female urethra, and the urethrovaginal sphincter, which areknown col- striated muscle of the urethra is predominantly slow twitch in lectively asthestriated urogenital sphincter muscle. The sphinc- nature. The striated muscle layer surrounds atwo-layered smooth terurethra encircles themidurethral wall,whereas thecompressor muscle component (CSM and LSM). Circularly arranged muscle urethra and sphincter urethrovaginalis arch over the distal cells occur in theouter aspect ofthesmooth muscle layer (CSM) urethra. The smooth muscle layers are highlighted in yellow. B. Illustration ofstriated muscle loss at the vulnerable zone ofthe and sometimes intermingle with thestriated muscle. The inner- urethra, at the bladder neck. Measurements oflayer thickness in most layer is longitudinally arranged (LSM). The urethral lamina our specimens showed thatthere was localized disappearance of propria (LP) extends from the longitudinal smooth muscle layer striated muscle, which contrasted with regions thatseemed more tothe urothelium and fills thelumen oftheurethra.The submu- resistant to damage.The pattern ofstriated muscle loss suggests cosa constitutes a relatively thick layer ofloosely woven connec- that striated muscle in the proximal and the dorsal wall ofthe tive tissue with a rich vascular supply. The urethral mucosa urethra might bemore vulnerable (arrows) toone ormore insults consists ofatransitiocellular epithelium in theproximalthird. This orprocesses than thedistal urethra. epithelium fades outin a regular squamous mucosal epithelium in thedistal two thirds oftheurethra. Collagen isthemajor struc- The Urethra tural component oftheconnective tissue in thefemale urethra, The adult female urethra is a complex 2-4-cm- whereas elastic fibers are exceedingly rare. LA =levator ani, V= long fibromuscular tube with a diameter of anterior vaginal wall, PU =pubourethralligaments. approximately 1cm, and it extends from the bladder neck to the external urinary meatus (Fig.

1.1. Functional Anatomy ofthe Pelvic Floor and Lower Urinary Tract 7 Urethral closure function, as measured by ure- During times of urgent need, the striated thral resting pressure, has been shown to decrease urogenital sphincter muscle increases closure with age,\" and groups of women with inconti- pressure by shortening its circumferentially ori- nence had statistically proven lower urethral ented muscle fibers and constricting the lumen. closure pressure than continent women.\" In addition, contraction of the pubococcygeal muscle results in urethra compression against The female urethra is composed of different adjacent tissue . This compression depends on the regions along its length and can be understood fascial attachment of the urethra to the levator by dividing the length of urethral lumen into ani muscle (Fig. 1.1.4). A blockade of striated fifths, each approximately 20% of the total muscle activity, on the other hand, decreases length .\" In the first quintile, the lumen of the resting urethral pressure by approximately 50%.18 urethra is surrounded by the vesical neck (0- Constantinou and Govan\" demonstrated that 20%). Next, the sphincter urethra and smooth during a cough a urethral pressure increase is muscle encircle the lumen from 20% to 60% of measurable at the level of the urethral sphincter, the total urethral length . The arch-shaped com- but not more proximally. This, together with pressor urethra and urethrovaginal sphincter are increased electro myographic activity during found from 60% to 80% of the total urethral cough and hold in healthy women,\" suggests length, whereas the distal component includes that the striated muscle does contribute to ure- only fibrous tissue and no significant contractile thral closure pressure. Muscle contraction is not elements (Fig. 1.1.3 A). always present in women with SUI, and some stress-incontinent women who are capable of Striated Urogenital Sphincter contracting their pelvic ft.oor on demand do not have a muscle contraction visible during a The outermost layer is composed of striated cough .\" muscle that has the following three components: (1) sphincter urethra, (2) compressor urethra, Urethral Smooth Muscle and (3) urethrovaginal sphincter. These compo- nents are collectively known as the striated uro- The striated muscle layer surrounds a two-layered genital sphincter muscle. The sphincter urethra smooth muscle component. The two layers of the encircles the midurethral wall, whereas the com- urethral smooth muscle consist of an outer cir- pressor urethra and sphincter urethrovaginalis cular layer (circular smooth muscle [CSM]) and arch over the distal urethra. Distally, under the an inner longitudinal layer (longitudinal smooth arch of the pubic bone, these fibers diverge muscle [LSM]) (Fig. 1.1.4). The circular fibers to insert into the walls of the vagina and the contribute to urethral constriction, and the perineal membrane (compressor urethra and smooth muscle blockade reduces resting urethral urethrovaginal sphincter) (Fig. 1.1.3 A). This closure pressure by approximately one third. The structure is often referred to as the external ure - function of the longitudinal muscle is not entirely thral sphincter. This muscle is responsible for understood. The longitudinal muscles are con- increasing intraurethral pressure during times of siderably vaster than circular muscles; the need, and it also contributes at least approxi- reasons for this have yet to be determined. mately one third of the resting tone of the urethra. Its composition of primarily slow-twitch, fatigue- The smooth muscle of the female urethra is resistant muscle fibers belies its constant activity. associated with relatively few noradrenergic The muscle cells are smaller than ordinary nerves, but it receives an extensive presumptive cholinergic parasympathetic nerve supply, which skeletal muscle cells, at approximately 20 urn in is identical in appearance to that which supplies the detrusor.\" The innervation and longitudi- diameter. 16 nal orientation of the majority of muscle fibers With increasing age, striated muscle loss at the suggest that the urethral smooth muscle in the female is active during micturition, serving to bladder neck and along the dorsal wall of the shorten and widen the urethral lumen . urethra (Fig. 1.1.3 B) has been found. This leads to a horseshoe-shaped aspect of the striated muscle layer in the midurethral cross section. \"

8 D. Perucchini and J.O.l. Delancey Urethral Submucosal Vasculature duloxetine, which is a selective serotonin and norepinephrine reuptake inhibitor.P:\" The submucosal vasculature is remarkably prom- inent and is far more extensive than one would Support ofthe Urethra and expect for such a small organ . It is likely respon- Pelvic Organs sible, in part, for the hermetic seal that maintains mucosal closure. Occlusion of arterial flow into Support of the urethra and pelvic organs rely on this area decreases resting urethral closure pres- their attachments to the pubic bones, muscles, sure ; therefore, these vessels are felt to participate and connective tissue of the pelvis. The female in closure function. \" pelvis and its supportive structures are not only important for micturition and defecation but Urethral Glands must also accommodate cohabitation, as well as vaginal birth. These demands on the female A series of glands are found in the submucosa, pelvic floor may lead to a series of problems and primarily along the dorsal (vaginal) surface of disorders. The pelvic floor consists of several the urethra.\" The glands are mostly concentrated components lying between the peritoneum and in the distal and middle thirds of the urethra, the perineum (Fig. 1.1.1). The support for all of varying in number and extent from one woman these structures comes from their connection to to the next. The location of urethral diverticula, the bony pelvis and its attached muscles by a which are derived from cystic dilation of these unique network of connective tissue. glands, follows this distribution, being most common distally and usually originating along The female pelvis can naturally be divided the dorsal surface of the urethra. into anterior and posterior compartments be- cause dense supportive tissues attach the pelvic Innervation ofthe Urethra organs to the lateral pelvic walls. The levator ani muscles form the bottom of the pelvis and are The innervation of the urethral sphincter com- U-shaped (Fig. 1.1.5). The vagina and the pelvic plex is controversial. Nerve stimulation studies showed early evidence that the external urethral FIGURE 1.1.5. Schematic view ofthe U-shaped levator ani muscle sphincter is innervated by the somatic fibers of from below, after the vulvar structures and perineal membrane the pudendal nerve. Several others have con- have been removed, showing the arcus tendineus levator ani cluded that the external sphincter receives its (AllA); external anal sphincter (EAS); puboanal muscle (PAM); innervation from the 52-53 spinal roots via perineal body (PS) uniting the2ends ofthepuboperineal muscle branches of the pudendal nerve .\" Others have (PPM); iliococcygeal muscle (lCM); puborectal muscle (PRM). reported that the sphincter complex also receives Note thattheurethra and vagina have been transected justabove autonomic innervation from the inferior hypo- thehymenal ring. (Source: Copyright © Delancey, 2003.) gastric plexus via intrapelvic fibers. A recent study found that stimulation of the intrapelvic portion of the cavernous nerves results in con- tractions of the urethral sphincter even after the bladder and urethra have been surgically divided. \" Although the importance of tonic sym- pathetic innervation to the male urethra has been well established, the role of sympathetic innerva- tion in women is only now being explored. The striated urethral sphincter is innervated by axons that originate from motor neurons in the sacral spinal cord and are carried into the pudendal nerve. The sphincter motor neurons are located in a circumscribed region of the sacral anterior horn called Onuf's nucleus. The poten- tial for pharmacologically increasing muscle tone in the urethra is suggested by recent studies of

1.1. Functional Anatomy ofthe Pelvic Floor and lower Urinary Tract 9 FIGURE 1.1.6. Bonney's analogy of vaginal prolapse. The eversion of an intussuscepted surgical glove finger by increasing pressure within theglove resultingisanalogous to prolapse ofthevagina. (Source: Delancey, 2002, with permission.) organ s are attached to the levator ani muscles by sure in the glove is increased, it forces the finger connective tissue when they pass through the to protrude downwards in the same way that urogenital hiatus and are supported by these increases in abdominal pressure force the vagina connections. The vagina has a similar relation- to prolapse. Vaginal support is a combination of ship to the abdominal cavity as that of the inverted constriction, suspension, and structural geome- finger of a surgical glove (Fig. 1.1.6).28If the pres- try. Figure 1.1.7 demonstrates this phenomenon FIGURE 1.1.7. Diagrammatic display ofvaginal support. (A)Invag- hiatus closed. (0) Ligament suspension. The vagina issuspended inated area in a surrounding compartment. (8) The prolapse from the pelvic walls, and pelvic floor muscle exercise does not opens when thepressure (arrow) isincreased. (C)The lower end directly affect thesuspension. (E) Flap valve closure where sus- ofthevagina isheld closed bythepelvicfloor muscles, preventing pending fibers holds the vagina in a position against the wall, prolapse byconstriction. Pelvic floormuscle exercise is, therefore, allowingincreases in pressure (arrows) to pinit in place. (Source: commonly recommended forprolapse with less severesymptoms Delancey, 2002, with permission.) and to prevent pelvic organ prolapse by keeping the urogenital

10 D. Perucchini and J.O.L. Delancey and the strategies that the body uses to prevent prolapse. Pelvic floor muscle exercise is commonly rec- ommended for prolapse with less severe symp- toms and to prevent pelvic organ prolapse by keeping the urogenital hiatus closed (Fig. 1.1.7 C). The Levator Ani Muscle Macroscopic Anatomy The major structural component of the pelvic FIGURE 1.1.9. Descending perineum syndrome. Damage to the floor is the levator ani muscle group because they levator ani muscle can result in visible descent of theperineum form the effective contractile support structure and enlarged hiatus. (Source: Delancey 2002, with permission.) of the region. Four muscles make up the levator ani: pubococcygeus, puborectalis, iliococcygeus, floor, and related organs in a cephalic direction and coccygeus. In practical terms, the pelvic floor (Figs. 1.1.5 and 1.1.8 A). Damage to the levator ani is synonymous with the levator ani. The opening muscle can lead to muscle weakness and to relax- within the levator ani muscle through which the ation of the pelvic floor, resulting in a visible urethra and vagina pass is called the urogenital descent of the perineum (descending perineum hiatus of the levator ani (Fig. 1.1.8). It is through syndrome) (Fig. 1.1.9). In women with normal this opening that genital prolapse occurs . Con- support and without previous surgery, the uro - stant adjustments in muscular baseline activity genital hiatus area is minimal. Increasing pelvic of the levator ani muscle\" keeps the urogenital hiatus closed, by compressing the vagina, urethra, and rectum against the pubic bone, the pelvic AB FIGURE 1.1.8. (AI All muscles of the pelvic floorinsert intothecoccyx. (B)The positionof thecoccyx varies because of pelvic floor muscle contraction orrelaxation.

1.1. Functional Anatomy ofthePelvic Floor and Lower Urinary Tract 11 organ prolapse is associated with per ineal descent External anal and increasing urogenital hiatus size. The hiatus is larger after several failed operations than after sphincter ---,~,<.::'\" successful surgery or single failure.\" FIGURE 1.1.11. lateral view ofthe pelvicfloor structures related to The bony coccyx is also influenced by the urethral support seen from theside in thestanding position, cut activity of the PFMs. All muscles of the pelvic just lateral tothemidline. Note thatwindows have been cut in the floor insert into the coccyx, and magnetic reso- levator ani muscles, vagina, and endopelvic fascia so that the nance imaging (MRI) studies have shown that urethra and anterior vaginal walls can beseen. (Source: Delancey, PFMcontractions lead to movement of the coccyx 2002, with permission; redrawn after Delancey, 1994.) in a ventral cranial direction, thereby contribut- ing to a closed urogenital hiatus (Fig. 1.1.8 B). and levator ani fascia and consist of dense aggre- During straining, the coccyx was pressed in a gations of connective tissue, predominantly col- caudal, dorsal direction, thus , facilitat ing the lagen, that provide lateral passive pelvic support. opening of the urogenital hiatus. \" The ATLA inserts at the anterior pubic rami bilaterally and at the posterior region at or near At the onset of micturition, the levator ani the ischial spine. The ATLA overlies the obtura- muscle relaxes, the urogenital hiatus opens, and tor internus muscle. The ATFP lies medial to the the vesical neck rotates downward to the limit of ATLA and inserts at the lower sixth of the pubic the elasticity of the fascial attachments. At the bone, 1em from the midline, and the posterior end of micturition, the levator an i muscle resumes region inserts into the ischium, just above the normal position and the urogenital hiatus is spine. closed . The levator ani muscle is composed of two The connective tissue covering the levator ani portions. The iliococcygeal muscle is a thin layer muscles on the superior and inferior surfaces are of muscle that spans the potential gap from one called the superior and inferior fascia of the pelvic sidewall to the other; it lies laterally and is levator ani. When these muscles and their associ- relatively flat horizontal in the standing position. ated fascia are considered together, the combined The iliococcygeal muscle originates at the ATLA, structures form the pelvic diaphragm. with a few fibers arising from the pubis. These fibers insert into the midline to form the anococ - Two prominent lateral conne ctive tissue struc- cygeal raphe midline between the anus and tures are important in supporting the levator ani coccyx. This region has also been called \"the muscle. The ATLA and the ATFP (Figs. 1.1.10 and levator plate.\" 1.1.11) are condensations of obturator intern us The more medial portions of the levator ani r / ' Parametnum (pubococcygeal and puborectal) form a sling Paracolptum (Fig. 1.1.5) that arises ventrally from the pubic bones and encircles the pelvic organs . It arises ~ Obturator mternus muscle Arcustendlneus levator ani - VeslC8l neck - - - - Levator a'\" ~\"'----Arcus ten<!,neus fasciae pelvis ' Ischoal spme FIGURE 1.1.10. Attachments ofthecervix and vagina tothepelvic walls demonstrating different regions ofsupport with theuterus in situ. Note thatthe uterine corpus and the bladder have been removed. (Source: Delancey, 2002, with permission.)

12 D. Perucchini and J.O.L. Delancey bilaterally from the pubis and wraps around the is a known adaptive response to inactivity, inner- midline structures of the bladder, urethra, vagina, vation damage, and ageing.\" During whole- and rectum, sending fibers to insert into the peri- muscle contraction, motor units are recruited in neal body, vagina, and anal sphincters, respec- order of increasing size.\" :\" A graded contraction tively. Various muscle subdivisions have been that proceeds from low to high intensity (weak to assigned to the medial portion of the pubococ- strong) begins with the recruitment of the type I cygeus to describe different visceral attachments motor units, followed by the recruitment type II of the muscle to the vagina (pubovaginalis), peri- units. In a muscle that is 30% type II fibers, neal body (puboperineus), and anus (puboana- such as in the pubococcygeus, 70% of the muscle lis). The puborectalis lies laterally and is not must be contracted before the type II units are considered a part of the pubococcygeal group recruited. To maintain the exercise training (puborectalis).\" effect, exercise physiology suggests that once initial muscle strengthening has occurred, a The obturator internus and piriformis are the reduced program of exercise can be adequate for major muscles of the pelvic sidewalls (Fig. 1.1.10). maintaining strength.\" The possible impact of The obturator internus is a large, fan-shaped age and parity on the pelvic floor has been studied muscle that arises from the bony margins of the by several authors .P:\" :\" They found that ageing obturator foramen, the pelvic surface of the obtu - and vaginal birth lead to histomorphologically rator membrane, and the rami of the ischium and visible changes that were consistent with changes pubis. This muscle forms the lateral wall of the of myogenic origin. These changes were more pelvis and can be palpated transvaginally. The pronounced in the ventral part of the pelvic floor, piriformis muscles form the posterior wall of leading to the assumption that the ventral part is the pelvis. These muscles originate from the the most vulnerable part of the muscle. anterior and lateral aspect of the sacrum in its middle to upper portion, coursing through the Innervation ofthe Levator Ani Muscle greater sciatic foramen and inserting on the greater trochanter of the femur. The levator ani muscle is innervated by somatic nerve fibers that run in the pudendal nerve and Muscle Fiber Type and Muscle Physiology emanate primarily from sacral root S3 and, to a lesser extent , from S2and S4. The pudendal nerve The levator ani muscle is a striated muscle. The carries both, motor and sensory fibers. Initially, constant activity of this muscle is analogous to the pudendal nerve lies superior to the sacrospi- the postural muscles of the spine. Their continu- nous ligament that is lateral to the coccyx. The ous contraction is similar to the continuous nerve leaves the pelvis, crossing the ischial spine activity of the external anal sphincter muscle, to reach the ischiorectal fossa via the lesser sciatic and it closes the lumen of the vagina in a manner foramen . It extends forward in a fibrous tunnel similar to how the anal sphincter closes the anus. called Alcock's canal on the medial side of the This constant action eliminates any opening obturator internus muscle and distally gives rise within the pelvic floor and prevents prolapse. to branches, which supply the levator ani and the membranous urethra. Some variation occurs in The muscle fibers of the levator ani include the pudendal nerve peripheral anatomy. both, type I (slow twitch) and II (fast twitch) fibers. Fast-twitch fibers are metabolically suited Levator Ani Function and for more rapid , forceful contraction, and slow- Continence Mechanism twitch fibers are suited for providing sustained muscular tone. Gilpin et al.33 found that in women The levator ani muscles play a critical role in with no symptoms of urinary incontinence the maintaining continence during the increase of anterior pubococcygeus muscle had a 33% popu- abdominal pressure. P'\" :\" During normal abdom- lation of type II fibers and the posterior pubococ- inal pressure, it is postulated that the resting ure- cygeus had a 24% population of type II fibers. A thral closure pressure is maintained by the tone decrease in the percentage of type II fibers, along with an increase in the diameter of type I fibers,

1.1. Functional Anatomy ofthe Pelvic Floor and Lower Urinary Tract 13 of the smooth and striated sphincters, intraure- geal muscle is hypothesized to result in urethral thral blood pressure, and the tendency of the ure- compression against adjacent tissues. Magnetic thral epithelium to close through coaptation.Y \" :\" resonance imaging has shown that 11% of conti- In the event of a sudden or prolonged increase in nent primiparous women demonstrated a major intraabdominal pressure (such as during a cough loss of the pubococcygeal portion of the levator or laughter), bladder pressure may exceed resting ani muscle, with certain women showing evi- urethral pressure and result in leakage, unless dence of complete muscle loss.\" This observation compensated for by additional urethral closure offered the opportunity to compare increases in pressure. This additional closure pressure is urethral closure pressure in women with and thought to be primarily developed by the striated without intact pubococcygeal muscle. In consec- levator ani because of the time constraint required utive studies, it was found that the likelihood of for the smooth muscle contraction to take place increasing urethral pressure with PFM contrac- within the approximate half-second pressure rise tion was decreased by 50% in the women with associated with a cough. During stress, the con- loss of the pubococcygeus.\" nective tissue, via its attachment to the striated levator ani muscle, helps create a firm \"floor\" of Connective Tissue ofthe Pelvic Floor: support underlying the vagina and urethra, onto Endopelvic Fascia which the urethra is compressed by intraabdomi- nal pressure.\" This extrinsic continence mecha- On each side of the pelvis, connective tissue nism provides the additional closure pressure attaches the cervix and vagina to the pelvic wall necessary to augment urethral closure during (Figs. 1.1.10 and 1.1.11). This fascia forms a con- increased intraabdominal stress. The relative tinuous sheet-like mesentery extending from the contributions to urethral closure made by the uterine artery at its cephalic margin to the point striated urethral sphincter muscles and the at which the vagina fuses with the levator ani levator muscles have not yet been fully elucidated. muscles below. The body of connective tissue that Miller et a1.43 showed that a precisely timed voli- attaches the pelvic organs to the sidewall is called tional contraction of the PFM before and during endopelvic fascia, which is a heterogeneous group stressful activities has considerable potential of tissues including collagen, elastin, smooth for helping to prevent urine loss in mild to muscle , blood vessels, and nerves. The composi- moderate SUI. Pelvic floor muscle contraction tion of the endopelvic fascia reflects its combined in preparation for, and throughout, a cough can functions of neurovascular conduit and support- augment proximal urethra support during stress, ive structure. The part of the fascia that attaches thus, reducing the amount of dorsocaudal to the uterus is called the parametrium, and the displacement.\" part that attaches to the vagina is called the para- colpium (Fig. 1.1.10).46 Miller et a1.43 observed that some women with SUI reported immediate benefits from Kegel Del.ancey\" has introduced the concept of exercises within 1-2 days after learning them. dividing the connective tissue support in the However, this time span was too short for any anterior part of the pelvis into three levels (Fig. true strengthening to have taken place. The 1.1.12), with levels I, II, and III representing improvement was hypothesized to have come apical, midvaginal, and distal vaginal support, from the well-timed volitional use of the PFMs respectively. Although assigning these levels during an activity known to precipitate urine loss artificially divides what is actually a continuum (such as a cough) and not from the actual of connective tissue in the pelvis, dividing this strengthening of the muscles. The skill of a well- support into regions (levels) proves useful tool to timed volitional PFM contraction was termed understand how the loss of support at different \"The Knack.?\" Miller et al. showed that selected levels can correlate with different physical signs women with mild to moderate SUI could learn to and symptoms that accompany a cystocele, significantly reduce urine loss within one week enterocele, or rectocele. Damage to the upper by intentionally contracting the PFMs before and suspensory fibers of the paracolpium (level I) during a cough. Contraction of the pubococcy- results in uterine or vaginal vault prolapse

14 D. Perucchini and J.O.L. Delancey levator ani - - -- responsible for the diversity of clinically encoun- tered problems. FIGURE 1.1.12. levels of vaginal support after hysterectomy. level I (suspension) and II (attachment). In level I, the paracol- The interaction between the PFMs and the pium suspends thevagina from thelateral pelvic walls. Fibers of supportive ligaments is critical to pelvic organ level Iextend both vertically and posteriorly toward thesacrum. support. With proper function of the levator ani In level II, the vagina is attached to the arcus tendineus fasciae muscles, the pelvic floor rema ins closed and the pelvis and thesuperior fascia oflevator ani. In level III thevagina ligaments and fascial structures are under is directly attached without Intervening paracopium. (Source: minimal tension . The fasciae simply act to stabi- Delancey, 1992, with permission.) lize the organs in their position above the levator ani muscles. When the PFMs relax or are (Fig. 1.1.13 B). Damage to the level II and III por- damaged, the pelvic floor opens and the vagina tions of the vagina results in anterior prolapse lies between the high abdom inal pressure and (cystocele; Fig. 1.1.13 A) and posterior prolapse low atmospheric pressure. As a result, the vagina (rectocele; Fig. 1.1.13 C). These defects occur in must be held in place by the ligaments. Although varying combinations and these variations are the ligaments can sustain these loads for short periods, if the PFMs do not close the pelvic floor then the connective tissue will eventually fail, resulting in pelvic organ prolapse. Anterior Wall Support and the Urethra The anterior vaginal wall and urethra are inti- mately connected (Figs. 1.1.4, 1.1.5, and 1.1.11). Both PFMs and the pelvic fasciae determine the support and fixation of the urethra, and the activ- ity of the muscles has significant influence on the urethral support.\" Disruption of this supportive system will result in downward descent of the anterior vaginal wall. The layer of tissue that provides urethral support FIGURE 1.1.13. Illustration of different prolapse findings. Three move downward between the anterior and posterior supports. types ofmovement occur in patients with pelvic organ prolapse: (C)The posterior wall can protrude through theintroitus. This is (A) The anterior vaginal wall can protrude through theintroitus. called \"rectocele,\" This is called \"cystocele,\" (8) The cervix (or vaginal apex) can

1.1. Functional Anatomy ofthe Pelvic Floor and Lower Urinary Tract 15 FIGURE 1.1.14. (left) The attachment of the arcus tendineus rated from the arcus tendineus (arrows point to thesides ofthe pelvis to the pubic bone, the arcus tendineus pelvis (arrows). split). PS = pubic symphysis. (Source: Delancey, 2002, with (Right) Aparavaginal defect where the cervical fascia has sepa- permission.) has two lateral attachments; a fascial attachment Richardson et al.,\" who observed that a lateral and a muscular attachment.\" The fascial attach- detachment (lateral defect) of the connections of ment of the urethral supports connects the peri- this paravaginal fascia from the pelvic wall was urethral tissues and anterior vaginal wall to the associated with stress incontinence and anterior arcus tendineus fascia of the pelvis and has been prolapse (Figs. 1.1.14 and 1.1.15). The muscular called the paravaginal fascial attachments by attachment connects these same periurethral FIGURE 1.1.15. (left) Displacement \"cystocele\" where the intact on this side. (Right) Distension \"cystocele\" where the anterior anterior vaginal wall has prolapsed downward because of para- vaginal wall fascia has failed and the bladder is distending the vaginal defect. Note thattheright side ofthepatient's vagina and mucosa flattening out the vaginal tissues. (Source: Delancey cervix has descended more than theleft because ofalarger defect 2002, with permission.

16 D. Perucchini and J.O.L. Delancey Uterovaginal Support FIGURE 1.1.16. lateral view ofpelvic floor with the urethra and The cardinal and uterosacral ligaments attach the fascial tissues transected atthelevel oftheproximal urethra.The cervix and uterus to the pelvic walls.50•51 Together arrow indicates compression ofthe urethra by a downward force these tissues are referred to as the parametrium against the supportive tissues and illustrates the influence of (Fig. 1.1.10). The parametrium continues down- abdominal pressure on theurethra.(Source: Delancey, 1994, with ward over the upper vagina to attach it to the permission.) pelvic walls. At this location, it is called the para- colpium.\" The paracolpium provides support for tissues to the medial border of the levator ani the vaginal apex after a hysterectomy, and it has muscle (Fig. 1.1.4). These attachments allow the two portions. The uppermost portion of the para- levator an i muscle's normal resting tone to main- colpium consists of a relatively long sheet of tissue tain the position of the vesical neck, which is that suspends the superior aspect of the vagina supported by the fascial attachments. When the (Fig. 1.1.12, Level I) by attaching it to the pelvic muscle relaxes at the onset of micturition, it wall. This is true whether or not the cervix is allows the vesical neck to rotate downward to the present. In the midportion of the vagina (Fig. limit of the elasticity of the fascial attachments, 1.1.12, Level II), the paracolpium attaches the and then contraction at the end of micturition vagina laterally and more directly to the pelvic allows it to resume its normal position (Fig. 1.1.5). walls. This attachment stretches the vagina trans- Damage to the connective tissue integrity can versely between the bladder and rectum and has lead to prolapse.t' :\" funct ional significance. The structural layer that supports the bladder (\"pubocervical fascia\") does The vaginal wall, in turn, is supported by con- not exist as a separate layer from the vagina, but nections to the levator ani muscles laterally and rather, is composed of the anterior vaginal wall to the arcus tendineus fascia pelvis. Simulated and its attachment through the endopelvic fascia increases in abdominal pressure reveal that the to the pelvic wall (Figs. 1.1.4and 1.1.16). Similarly, urethra can be compressed against the vaginal the posterior vaginal wall and endopelvic fascia wall, acting as a supporting hammock (Fig. (rectovaginal fascia) form the restraining layer 1.1.16).10 In fact, it is the relative elasticity of this that prevents the rectum from protruding forward, supporting apparatus, rather than the height of thereby blocking formation of a posterior pro- the urethra, that results in stress incontinence. In lapse. In the distal vagina (Fig. 1.1.12,level III), the an individual with a firm supportive layer, the vaginal wall is directly attached to surrounding urethra would be compressed between abdomi- structures without any intervening paracolpium. nal pressure and pelvic fascia. If, however, the Anteriorly, it fuses with the urethra, and posteri- layer under the urethra becomes unstable and orly it fuses with the perineal body, and laterally does not provide a firm backstop for abdominal with the levator ani muscles (Fig. 1.1.12). pressure to compress the urethra against, the opposing force that causes closure is lost and the Prolapse of the uterus or the vagina after a occlusive action diminished. hysterectomy has been performed is common. The nature of uterine support can be understood when the uterine cervix is pulled downward with a tenaculum in an anesthetized pelvic surgery patient. After a certain amount of descent, the parametria become tight and arrest further cer- vical descent . Similarly, descent of the vaginal apex after hysterectomy is resisted by the para- colpia. The inability of these ligaments to deter- mine the resting position of the uterine cervix in normal healthy women is supported by the obser- vation that the cervix may be drawn down to the level of the hymen with little difficulty.52

1.1. Functional Anatomy ofthe Pelvic Floor and lower Urinary Tract 17 Perineal Membrane (Urogenital Diaphragm) f and External Genital Muscles FIGURE 1.1.17. The perineal membrane spans the arch between In the anterior pelvis, below the levator ani theischiopubicrami, with each side attached totheother through muscles, there is a dense , triangularly shaped their connection in the perineal body. Note that separation membrane called the per ineal membrane. The of the fibers in this area leaves the rectum unsupported and term perineal membrane replaces the old term results in a low posterior prolapse. (Source: Delancey, 1999, with \"urogenital diaphragm,\" reflecting the fact that permission.) this layer is not a single layer with a \"diaphragm,\" but rather a set of connective tissues that sur- the levator ani muscles. 54 The lower third of the round the urethra.53 The perineal membrane lies vagina is fused with the perineal body (Fig. 1.1.17). at the level of the hymenal ring and attaches the This structure is the attachment between the per- urethra, vagina, and perineal body to the ischio- ineal membranes on either side of it, and this pubic rami (Fig. 1.1.17). The compressor urethra connection prevents downward descent of the and urethrovaginal sphincter muscles are associ- rectum in th is region. If the fibers that connect ated with the upper surface of the perineal mem- one side with the other rupture (Fig. 1.1.18 A) then brane (Figs. 1.1.1 and 1.1.3 A). Previous concepts the bowel may protrude downward, resulting in a of the urogenital diaphragm show two fascial posterior vaginal wall prolapse (Fig. 1.1.18 B). The layers with a transversely oriented muscle, the midposterior vaginal wall (Fig. 1.1.12, Level II) is \"deep transverse perineal muscle,\" in between connected to the inside of the levator ani muscles them . Observations based on serial histology and anatomic dissection, however, reveal a single connective tissue membrane, with the compres- sor urethra and urethrovaginal sphincter lying immediately above. These striated muscles have the largest bulk of the striated urogenital sphinc- ter, and thi s fact explains why pressures during a cough are greatest in the distal urethra,\" :\" where they can compress the lumen closed in anticipa- tion of a cough .v\" Posterior Support The posterior vaginal wall is supported by con- nections between the vagina, the bony pelvis, and /1 I/ A FIGURE 1.1.18. (Aand B) Posterior prolapse caused by separation vagina, no longer united with its companion on the other side oftheperineal body (A). (Delancey, 2002, with permission). Note (arrows) (B). the end ofthe hymenal ring thatlies laterally ontheside of the

18 D. Perucchini and J.O.L. Delancey by sheets of endopelvic fascia. These connections continence. The anal sphincter complex is com- prevent the ventral movement of the vagina posed of the internal and external anal sphincter during increases in abdominal pressure. muscle and contains both smooth and striated muscle (Fig. 1.1.19). The internal anal sphincter The attachment of the levator ani muscles into muscle is a continuation of the circular smooth the perineal body is important. Damage to this muscle layer of the rectum. The external anal part of the levator ani muscle during delivery is sphincter surrounds the internal sphincter in its one of the irreparable injuries to pelvic floor (Fig. lower 2ern by a muscular component that is teth- 1.1.18 B). Recent MRI has vividly depicted these ered to the coccyx through the anococcygeal defects, showing that up to 20% of nulliparous raphe .55 Immediately cephalic and anterior to the women have a visible defect in the levator ani external sphincter is the puborectalis muscle. muscle on MRI.40 This muscular damage is likely The striated external anal sphincter muscle pro- an important factor associated with the recur- vides voluntary squeeze tone to the sphincter rence of pelvic organ prolapse after initial surgi- complex. The external anal sphincter is classi- cal repair. Moreover, these defects were found to cally described as having three portions: deep, occur more frequently in those individuals com- superficial, and subcutaneous. plaining of stress incontinence. An individual with malfunctioning muscles has a problem that The internal anal sphincter contributes ap- is not surgically correctable. A more complete proximately 75% of the maximum anal resting understanding of the pelvic floor biomechanics is pressure; 25% comes from the external anal needed to understand the structural effects of sphincter. If there is sudden distention, the exter- these lesions better. nal anal sphincter can contribute up to 60% of the anal canal pressure for a short time, but it Anatomy ofthe Anal cannot maintain sustained tone. Resting and Sphincter Complex squeezing anal pressures decline with ageing.56 Fecal incontinence is a devastating condition, Between the internal and external anal sphinc- which is often associated with childbirth. The ter is the intersphincteric groove. This space anal sphincter complex and the puborectalis receives the downward extension of the conjoined muscle provide the majority of control of anal fibers of the levator ani muscles. These fibers suspend and elevate the anorectum, preventing its downward prolapse. Rectum Circula r sm oo th muscle IIwc occyg~ Levator ani { Puborcc/Qlis Dt:t:P External Supcr[u:ral anal { spbincter Subcu taneous FIGURE 1.1.19. Diagrammatic representa- tion of the anal sphincter mechanism. (Thakar and Sultan, 2003.)

1.1. Functional Anatomy ofthePelvic Floor and Lower Urinary Tract 19 The external anal sphincter is innervated by urinary bladder by cAMP. Eur I Pharmacol. S2-S4 fibers that travel via the inferior hemor- 2000;404:273-280. rhoidal portion of the pudendal nerve. The 6. Deng FM, Ding M, Lavker RM, et al. Urothelial puborectalis muscle, as previously described, function reconsidered: a role in urinary protein forms a V-shaped loop that begins from the pubic secretion. Proc Natl Acad Sci USA. 2001;98:154- bones and passes behind the rectum. The muscle 150. has constant muscular activity and is relaxed 7. Gil Vernet, S. Morphology and function of the only at the time of defecation. It also acts by vesico-prostato-urethral musculature. Edizioni causing a kink in the rectum, so that there is a Canova, Treviso, 1968. 90° angle between the anal and rectal canals. The 8. Mcguire EI. The innervation and function of the contraction of this muscle can be assessed by the lower urinary tract. I Neurosurg. 1986;65(3):278- degree to which the anus is elevated (\"levator 285. ani\") and pulled inward when the patient con- 9. DeLancey 10. Structural aspects of the extrinsic tracts her pelvic muscles. continence mechanism. Obstet Gynecol. 1988;72; 296-301. Conclusion 10. DeLancey 10. Structural support of the urethra as it relates to stress urinary incontinence: the A series of factors are important to urinary and hammock hypothesis. Am I Obstet Gynecol. 1994; fecal continence and to the normal support of the 170:1713-1720. female pelvic organs . Many advances are yet to 11. Wilson PD, Dixon IS, Brown AD, et al. Posterior be made concerning the pelvic floor, the conti- pubo-urethral ligaments in normal and genuine nence mechanism, and prolapse. Current and stress incontinent women. I Urol. 1983;130(4):802- future researchers should aim to uncover the 805. faults that are certainly present in the current 12. Huisman AB. Aspects on the anatomy of the paradigms so that prevention and treatment of female urethra with special relation to urinary pelvic floor disorders can pass from its cur- continence. Contrib Gynecol Obstet. rent phase of clinical empiricism to scientific 1983;10:1-31. certainty. 13. Rud T. Urethral pressure profile in continent References women from childhood to old age. Acta Obstet Gynecol Scand. 1980;59:331-335. I. Olsen AL, Smith VI, Bergstrom 10. Epidemiology of surgically managed pelvic organ prolapse and 14. Hilton P, Stanton, SL. Urethral pressure measure- urinary incontinence. Obstet Gynecol. 1997;89(4): ment by micro transducer: the results in symptom- 501-506. free women and in those with genuine stress incontinence.BrI ObstetGynaecol.I983;90(l0):919- 2. Mant I, Painter R, Vessey M. Epidemiology of 933. genital prolapse: observations from the Oxford 15. DeLancey 10. Correlative study of paraurethral family planning association study. Br I Obstet anatomy. Obstet Gynecol. 1986;68:91-97. Gynaecol. 1997;104(5):579-585. 3. Perucchini D, DeLancey 10, Ashton Miller I, et al. 16. Gosling lA, Dixon IS, Critchley HO, et al. A com- Age effects on urethral striated muscle I. Changes in number and diameter of striated muscle fibers parative study of the human external sphincter in the ventral urethra. Am I Obstet Gynecol. and periurethral levator ani muscles. Br I Urol. 2002;186:351-355. 1981;53(1):35-41. 4. Nygaard IE, Thompson FL, Svengalis SL, Albright 17. Perucchini D, DeLancey 10, Ashton Miller I, et al. IP. Urinary incontinence in elite nulliparous ath- Age effects on urethral striated muscle II. Ana- letes. Obstet Gynecol. 1994;84:183-187. tomic location of muscle loss. Am I Obstet Gynecol. 5. Burton TI, Elneil S, Nelson CP, et al. Activation of 2002;186:356-360. 18. Thind P, Bagi P, Mieszczak C, et al. Influence of epithelial Na(+) channel activity in the rabbit pudendal nerve blockade on stress relaxation in the female urethra. Neurourol Urodyn . 1996;15: 31-36. 19. Constantinou CE, Govan DE. Spatial distribution and timing of transmitted and reflexly generated urethral pressures in healthy women. I Urol. 1982; 127(5):964-969. 20. Constantinou, CEo Resting and stress urethral pressures as a clinical guide to the mechanism of

20 D. Perucchini and J.O.L Delancey continence in the female patient. Urol Clin N Am. in patients with pelvic relaxation and genuine 1985;12(2):247-258. stress incontinence. Obstet Gynecol.1989;74(5):789- 21. Bump RC, Hurt WG, Pantl JA, et al. Assessment of 795. Kegel pelvic muscle exercise performance after 35. Henneman E, Somjen C, Carpenter D. Functional brief verbal instruction. Am J Obstet Gynecol. significance of cell size in spinal motor neurons. 1991;165(2):322-327. J Neurophysiol. 1965;28:561-580. 22. Ek A, AIm P, Andersson K-E, et al. Adrenergic 36. Henneman E, Somjen G, Carpenter D. Excitability and cholinergic nerves of the human urethra and inhibitibility of motoneurons of different and urinary bladder. A histochemical study. Acta sizes. J Neurophysiol. 1965;28:599-620. Physiol Scand. 1997;99:345. 37. Graves JE, Pollock ML, Leggett SH, et al. Effect of 23. Huffman, J. Detailed anatomy of the paraurethral reducing training frequency on muscular strength. ducts in the adult human female. Am J Obstet Inter J Sports Med. 1988;9:316-319. Gynecol 1948;55:86. 38. Jundt K, Kiening M, Fischer P, et al. Is the histo- 24. Juenemann, KP, Lue TF, Schmidt RA, et al. Clini- morphological concept of the female pelvic floor cal significance of sacral and pudendal nerve and its changes due to age and vaginal delivery anatomy. J Urol. 1988;139(l):74-80. correct? Neurourol Urodyn . 2005;24:44-50. 25. Nelson CP, Montie JE, Mcguire EJ, et al. Intra- 39. Dimpfl T, Jaeger C, Mueller-Felber W, et al. Myo- operative nerve stimulation with measurement genic changes of the levator ani muscle in pre- of urethral sphincter pressure changes during menopausal women: the impact of vaginal delivery radical retropubic prostatectomy: a feasibility and age. Neurourol Urodyn. 1998;17(3):197-205. study. J Urol. 2003;169(6):2225-2228. 40. DeLancey JOL, Kearney R, Chou Q, et al. The 26. Thor KB. Serotonin and norep inephrin involve- appearance oflevator ani muscle abnormalities in ment in efferent pathways to the urethral rhabdo- magnetic resonance images after vaginal delivery. sphincter: implication for treating stress urinary Obstet Gynecol. 2003;101:46-53. incontinence. Urology. 2003;62:3-9. 41. Petros PEP, Ulmsten UL. An integral theory of 27. Millard RJ, Moore K, Rencken R, et al. Duloxetine female urinary incontinence. Experimental and UI study group. Duloxetine vs, placebo in the clinical considerations. Acta Obstet Gynecol treatment of stress urinary incontinence: a four - Scand. 1990;153:7-31. continent randomized trial. BJU Int. 2004;93 :311- 42. Pandit M, DeLancey JO, Ashton-Miller J, et al. 318. Quantification of intramuscular nerves within 28. Bonney V. The principles that should underlie all the female striated urogenital sphincter muscle. operations for prolapse. Obstet Gynaecol Br Emp. Obstet Gynecol. 2000 ;95:797-800. 1934;41:669. 43. Miller JM, Ashton-Miller JA, DeLancey JO. A 29. Taverner D. An electromyographic study of the pelvic muscle precontraction can reduce cough- normal function of the external anal sphincter related urine loss in selected women with mild and pelvic diaphragm. Dis Colon Rectum . 1959;2: SUI. J Am Geriatr Soc. 1998;46:870-874. 153-158. 44. Miller JM, Perucchini D, Carchidi LT, et al. Pelvic 30. DeLancey JO, Hurd WW. Size of the urogenital floor muscle contraction during a cough and hiatus in the levator ani muscles in normal women decreased vesical neck mobility. Obstet Gynecol. and women with pelvic organ prolapse . Obstet 2001;97:255-260. Gynecol. 1998;91(3):364-368. 45. Miller JM, Umek WH, DeLancey JO, et al. Can 31. Bo K, Lilleas F, Talseth T, et al. Dynamic MRI of women without visible pubococcygeal muscle in the pelvic floor muscles in an upright and MR images still increase urethral closure pres- sitting position. Neurourol Urodyn . 2001;20:167- sures? Am J Obstet Gynecol. 2004;191:171-175. 174. 46. DeLancey JO. Anatomic aspects of vaginal ever- 32. Kearney R, Shawney R, DeLancey JO. Levator ani sion after hysterectomy. Am J Obstet Gynecol. muscle anatomy evaluated by origin-insertion 1992;166:1717-1728. pairs. Obstet Gynecol. 2004;104(l):168-173. 47. Richardson AC,Edmonds PB, Williams NL. Treat- 33. Gilpin SA, Gosling JA, Smith AR, et al. The patho- ment of stress ur inary incontinence due to para- genesis of genitourinary prolapse and stress vaginal fascial defect. Obstet Gynecol. 1981;57:357- incontinence of urine. A histologic and histo- 362. chemical study. Br J Obstet Gynaecol. 1989;64(4): 48. DeLancey JOL. Fascial and muscular abnormali- 385-390. ties in women with urethral hypermobility and 34. Koelbl H, Strassegger H, Riss PA, et al. Morpho- anterior vaginal prolapse. Am J Obstet Gynecol. logic and functional aspects of pelvic floor muscles 2002;18:93-98.

1.1. Functional Anatomy ofthePelvic Floor and Lower Urinary Tract 21 49. Halban J, Tandler I. Anatomie und Aetiologie der 54. DeLancey JO. Structural anatomy of the posterior Genitalprolapse beim Weibe. Vienna, Austria: pelvic compartment as it relates to rectocele. Am Wilhelm Braumuller, 1907. J Obstet Gynecol. 1999;180:815-823. 50. Campbell RM. The anatomy and histology of the 55. DeLancey JOL, Toglia MR, Perucchini D. Internal sacrouterine ligaments. Am J Obstet Gynecol. and external anal sphincter anatomy as it relates 1950;59:1. to midline obstetrical lacerations. Obstet Gynecol. 1997;90:924-927. 51. Range RL, Woodburne RT. The gross and micro- scopic anatomy of the transverse cervical liga- 56. Haadem K, Dahlstrom JA, Ling 1. Anal sphincter ments . Am J Obstet Gynecol. 1964;90:460-462. competence in healthy women . Clinical implica- tion of age and other factors . Obstet Gynecol. 52. Bartscht KD, DeLancey JO. A technique to study 1991;78:823-827. the passive supports of the uterus. Obstet Gynecol. 1988;72(6):940-943. 53. Oelrich TM. The striated urogenital sphincter muscle in the female. Anat Rec. 1983;205:223-232.

1.2 Neural Control of Pelvic Floor Muscles David B. Vodusek Key Message A clear understanding of anatomy and the neural control of the PFM and related visceral The coordinated function of pelvic floor muscles organs, as well as an insight into neuromuscular (PFM) and related organs is an important pre- damage and repair, is needed for planning suc- requisite that enables women to be continent of cessful PFM treatment in the individual patient urine and feces, to micturate and defecate, and to for any dysfunctional pelvic floor disorder. Par- experience orgasm. It is dependent on a complex ticularly in stress urinary incontinence, the acti- neuro control consisting of voluntary muscle vation and coordination disturbances of PFMare actions and reflexes, genetically determined clinically relevant. Proper identification of such activation patterns allowing for a meticulous PFM disturbances should lead to better selection interplay of skeletal and autonomous muscle of patients for particular modes of treatment and structures, and related organs. This scientifically to an improvement in the outcomes of conserva- complicated material is broken down in this tive treatments. chapter to a very understandable and practical level, which is a basic necessity for sophisticated Pelvic Floor Muscle Activity pelvic floor physiotherapy. Introduction Muscles do not really have much activity of their own. They are dependent on neural control. The Neural control of pelvic organs is affected by a \"denervated\" muscle atrophies and turns into unique coordination of the somatic and auto- fibrotic tissue. As every tissue muscle consists of nomic motor nervous systems. Pelvic floor cells (muscle fibers). However,the functional unit muscles are intimately involved in the function within a striated muscle is not a single muscle of the LUTand the anorectum, as well as in sexual cell, but a motor unit. A motor unit consists of funct ion. The neural control of the participation one alpha (or \"lower\") motor neuron (from the of striated muscle in \"visceral activity\" tran- motor nuclei in the brainstem or spinal cord), scends the simple somatic innervation necessary and all the muscle cells that this motor neuron for control of striated muscles functioning alone. innervates. In other words, the motor unit is the Sensory information and feedback to pelvic floor basic functional unit of the somatic motor system, organs is supplied by both visceral and somatic and control of a muscle means control of its sensory fibers, which also influence pelvic floor motor units. Thus, in discussing neural control muscle excitability thresholds through central of muscle, we only need to consider the motor integrative mechanisms. neurons in the spinal cord and all the influences they are exposed to. 22

1.2. Neural Control ofPelvic Floor Muscles 23 The function of pelvic floor and sphincter 1s lower motor neurons is organized quite differ- ently from other groups of motor neurons. In ~1mv contrast to the reciprocal innervation that is common in limb muscles, the neurons innervat- 1ms ing each side of the PFM have to work in harmony and synchronously. Thus, they achieve the FIGURE 1.2.2. Afalling leaf display ofa continuously firing tonic \"closure unit\" of the excretory tracts, the \"support motor unit.The vertical intervals between thebeams indicate the unit\" for pelvic viscera, and an \"effector unit\" in interval between two consecutive activations ofthe motor unit. the sexual response. In general, the muscles The regularity ofthemotor unit discharge should benoted. (From involved in the above functions act in a strictly theurethral sphincter ofacontinent 46-year-old woman.)(Source: unified fashion as \"one muscle,\" as has been dem- Schussler et al, 1994.) onstrated not only in sphincter muscles but also for both pubococcygeus muscles .' 1.2.1). This differs between individuals and also continues after subjects fall asleep.' This phy- However, as each muscle in the pelvis has its siological spontaneous activity may be called own unilateral peripheral innervation, dissoci- \"tonic,\" and it depends on prolonged activation ated activation patterns are also possible and of certain tonic motor units (Figs. 1.2.2 and have been reported between the two pubococ- 1.2.3).5 As a rule, it increases with bladder filling, cygeus/ and between the levator ani and the ure- thral sphincter.' The differences in evolutionary origin of the sphincter muscles and levator ani further imply that unilateral activation may be less of an impos- sibility for the PFMs than for sphincters. It can be postulated that the neural mechanisms controlling the different muscles involved in sphincter mecha- nisms and pelvic organ support may not be as uniform as has been assumed. How much variabil - ity there is in the normal activation patterns of the PFMis not yet clarified. It is clear, however, that the coordination between individual PFMscan defini- tively suffer because of disease or trauma. Tonic and Phasic Pelvic Floor Muscle Activity The normal striated sphincter muscles demon- strate some continuous motor unit activity at rest, as revealed by kinesiological EMG (Fig. ] 200UV t t Tonic activity t Cough Pinp rick Voluntarycontraction FIGURE 1.2.1. Kinesiological EMG recordings from urethral sphincter muscle. Concentric needle electrode recording in a continent 53-year-old female; recruitment ofmotor units onreflex maneuvers and oncommand to contract. (Source: Schussler et al., 1994.)

24 0.8. Vodusek (n) is encountered in many, but not all, detection sites for the levator ani muscle' :' and is practically 250 never seen in the bulbocavernosus muscle. ' In the pubococcygeus of the normal female there is - some increase of activity during bladder filling, and reflex increases in activity during any activa- 200 f0- tion maneuver performed by the subject, e.g., r- talking, deep breathing, and coughing. 150 - On voiding, inhibition of the tonic activity of the external urethral sphincter, and the PFM, r- f- leads to relaxation. This can be detected as a disappearance of all EMG activity, which pre- 150 rt cedes detrusor contraction. Similarly, the stri- ated anal sphincter relaxes with defecation and - 10Hz micturition.\" 50 Reflex Activity ofPelvic Floor Muscles o r-rf As the human urethral and anal striated sphinc- ters seem to have no muscle spindles, their reflex 3 45 reactivity is, thus, intrinsically different from the levator ani muscle complex, in which muscle FIGURE 1.2.3. Frequency histogram of the discharge rate of a spindles and Golgi tendon organs have been dem- continuously firing tonic motor unitfrom theanal sphincter of a onstrated.' Thus, PFM have the intrinsic proprio- healthy adult female. The values ontheyaxis denote thenumber ceptive \"servomechanism\" for adjusting muscle of discharges (n) . The regularity of the motor unit discharge length and tension, whereas the sphincter muscles should benoted. (Schussler etaI., 1994.) depend on mucosa and afferents from skin. Both muscle groups are integrated in reflex activity while depending on the rate of filling. Any reflex that incorporates pelvic organ function. or voluntary act ivation is mirrored first in an increase of the firing frequency of these motor The reflex activity of the PFM is clinically and units. On the contrary, inhibition of firing is electrophysiologically evaluated by eliciting the apparent on initiation of voiding (Fig. 1.2.4). bulbocavernosus and anal reflexes. The bulbo- cavernosus reflex is evoked on nonpainful dorsal With any stronger activation or sudden increase clitoral nerve stimulation. As recorded by EMG, in abdominal pressure (e.g., coughing), and only it is a complex response; its first component is for a limited length of time, new motor units are thought to be an oligosynaptic reflex and the later recruited and may be called \"phasic\" motor units. component a polysynaptic reflex.\" The polysyn- As a rule, they have potentials of higher ampli- aptic anal reflex is elicited by pinprick stimula- tudes and their discharge rates are higher and tion in the perianal region . irregular. A small percentage of motor units with an \"intermediate\" activation pattern can also be encountered.S (It must be stressed that this typing of motor units is electrophysiological, and that no direct correlation to histochemical typing of muscle fibers has so far been achieved .) In regard to tonic activity, sphincters differ from some other perineal muscles; tonic activity J 200JlV t 1s Tonic Activity FIGURE 1.2.4. Inhibition of firing of tonic muscle activity on when thecommand was terminated (from theurethral sphincter command (to fake micturition). The arrow indicates the point at of acontinent 53-year-old woman). which thecommand was given; thedouble arrowheads indicate

1.2. Neural Control of Pelvic Floor Muscles 2S The constant tonic activity of sphincter muscles cally, feedback on limb muscle function (acting is thought to be the result of the characteristics at joints) is derived not only from their input of their \"low threshold\" motor neurons and from muscle spindles, and receptors in tendons, the constant reflex inputs either of segmental but also from the skin , from visual input, etc. or of suprasegmental origin. It is supported \"Awareness,\" in fact, overlaps with the ability to by cutaneous stimuli, pelvic organ distension, voluntarily change the state of a muscle. and intraabdominal pressure changes . Sudden increases in intraabdominal pressure, as a rule, In contrast to limb muscles, PFMs and sphinc- lead to brisk reflex activity, which has been called ters lack several of the aforementioned sensory the \"guarding reflex\"; it is organized at the spinal input mechanisms and, hence, the brain is weakly level. informed about their status. Additionally, there is a gender difference , inasmuch as PFM aware- To correspond to their functional (effector) ness in females seems to be generally less deve- roles as pelvic organ supporters (e.g., during loped compared with males. Although nearly all coughing or sneezing), as sphincters for the lower healthy males are able to voluntarily contract urinary tract (LUT) and anorectum, and as an the pelvic floor, roughly every fourth healthy effector in the sexual arousal response, orgasm, woman lacks this ability. The need for \"squeezing and ejaculation, PFM also have to be involved in out\" the urethra at the end of micturition, as well very complex involuntary reflex activity, which as the close relationship of penile erection and coordinates the behavior of pelvic organs (smooth ejaculation with pelvic floor function, seems to muscle) and several different groups of striated be the origin of this difference. This primarily muscles. This activit y is to be understood as orig- weak or absent awareness of PFM in women inating from so-called \"pattern generators\" seems to be further jeopardized by vaginal within the central nervous system, particularly delivery. the brainstem. These pattern generators (\"reflex centers\") are genetically built-in and are respon- To regain awareness (or initiate it if it had pri- sible for complex reflex motor activity. marily been weak or absent) follows the same principles as any other motor rehabilitation. Motor learning has to aim for the activation of a \"dormant\" pattern generator. Muscle Awareness The sense of position and movement of one's Voluntary Activity ofPelvic Floor Muscles body is referred to as proprioception, and it is particularly important for sensing limb posi- Skilled movement of distal limb muscles requires tion (stationary proprioception) and movement individual motor units to be activated in a highly (kinesthetic proprioception). Proprioception focused manner by the primary motor cortex. In relies on special mechanoreceptors in muscle contrast, the activation of axial muscles (neces- tendons and joint capsules. In muscles, there are sary to maintain posture, etc.), while also under specialized stretch receptors, called muscle spin- voluntary control, depends particularly on ves- dles, and in tendons there are Golgi tendon tibular nuclei and reticular formation to create organs, which sense the contractile force. In addi- predetermined \"motor patterns.\" tion , stretch-sensitive receptors signaling pos- tural information are also in the skin , and this PFM are, in principle, under voluntary control, cutaneous proprioception is particularly impor- i.e., it is possible to voluntarily activate or inhibit tant for control of the movements of muscles the firing of their motor units (Figs. 1.2.1 and without bony attachment (e.g., lips and anal 1.2.4). There have been some claims that the sphincter). sphincter muscles can be contracted voluntarily, but not relaxed at will. EMGstudies have shown, Thus, the functional status of a str iated muscle however, that the activity of motor units in (or rather a certain movement) is represented in the urethral sphincter can be extinguished at the brain. Indeed, muscle awareness reflects the both low and high bladder volumes , even with- amount of sensory input from various sites. Typi- out initiating micturition.v \" Nevertheless, the

26 0.8. Vodusek voluntary control of both the sphincter and other Innervation ofPelvic Floor Muscles perineal muscles and PFMs is not as straight- Somatic Motor Pathways forward, unconditional, and reliable as it is for limb muscles. It is well known that many other- The motor neurons that innervate the striated wise neurologically healthy women cannot con- muscle of the external urethral and anal sphinc- tract their PFMs on command, which is also ters and perineum originate from a localized demonstrated by EMG recordings. Thus, the column of cells in the sacral spinal cord called voluntary control of these muscles seems to be Onuf's nucleus. \" In humans, it expands from the less straightforward, and maybe more fragile second to third sacral segment (S2-S3), and occa- than is commonly the case with striated limb sionally into Sl.I4Within Onuf's nucleus there is musculature. some spatial separation between motor neurons concerned with the control of the urethral and of In order to voluntarily activate a striated the anal sphincter (Fig. 1.2.5). muscle we have to have the appropriate brain \"conceptualization\" of that particular movement, Spinal motor neurons for the levator ani group which acts as a rule within a particular complex of muscles seem to originate from S3-S5 seg- \"movement pattern.\" This evolves particularly ments and show some overlap.\" through repeatedly executed commands and re- presents a certain \"behavior.\" Sphincter motor neurons are uniform in size and smaller than the other alpha motor Proprioceptive information is crucial for stri- neurons. They also differ with respect to their ated muscle motor control, both in the \"learn ing\" high concentrations of amino acid-, neuropep- phase of a certain movement and for later execu- tide-, norephinephrine-cserotonin-,and dopamine- tion of overlearned motor behaviors. Propriocep- containing terminals; these represent the tive information is passed to the spinal cord by fast-conducting, large-diameter myelinated FIGURE 1.2.5. The pudendal nerve isderived from ventral rami of afferent fibers and is influenced not only by the roots (51, 52, 53, and 54). It continues through thegreater sciatic current state of the muscle but also by the efferent foramen and enters in a lateral direction into the ischiorectal discharge the muscle spindles receive from the fossa. Itsmuscular branches innervatetheexternal anal sphincter nervous system via gamma efferents. In order to and the external urethral sphincter. There may be muscular work out the state of the muscle, the brain must branches for the levator ani, which is, as a rule, innervated by take into account these efferent discharges and direct branches from thesacral plexus (from above). which isthe make comparisons between the signals it sends out to the muscle spindles along the gamma effer- levator ani nerve. EA5 =external anal sphincter; EU5 =external ents and the afferent signals it receives from the = =urethral sphincter, LAN levator ani nerve, MLA musculus primary afferents. Essentially, the brain com- levator ani, PN =pudendal nerve. (Source : Modified from Swash, pares the signal from the muscle spindles with the copy of its motor command (the \"corollary 2002.)41 discharge\" or \"efferents copy\"), which was sent to the muscle spindle intrafusal muscle fibers by the central nervous system via gamma efferents. The differences between the two signals are used in deciding on the state of the muscle . Experi- ments were done in limb muscles, \" but it has been suggested\" that similar principles rule in bladder neurocontrol; the brain would know which efferent discharges were caused by disten- sion and which were caused by contractions because the latter would be initiated by the central nervous system. We propose that this is generally true, but that the mechanism, while present, is quite \"weakly developed\" for PFMs.

1.2. Neural Control ofPelvic Floor Muscles 27 substrate for the distinctive neuropharmacologic and sexual) functions. It should be mentioned responses of these neurons, which differ both that PFM need to not only be neurally coordi- from those of limb muscles, the bladder, and the nated \"within\" a particular function (for instance, PFM. with bladder activity), but the single functions need to be neurally coordinated with each other The somatic motor fibers leave the spinal cord (e.g., voiding and erection). at the ventral radices and fuse with the dorsal radices to constitute the spinal nerve. After The aforementioned sacral function control passing through to the intravertebral foramen, system is proposed to be a part of the \"emotional the spinal nerve divides into a dorsal ramus and motor system.\" This is a system derived from a ventral ramus.\" Somatic fibers from the ventral brain or brainstem structures belonging to the rami (also called the sacral plexus) form the limbic system. It consists of a medial and a lateral pudendal nerve. Traditionally, the pudendal component.\" The medial component represents nerve is described as being derived from the S2- diffuse pathways originating in the caudal brain- S4 ventral rami, but there may be some contribu- stem and terminating on (almost all) spinal grey tion from the S1, and possibly little or no matter, using serotonin in particular as its neu- contribution from the S4.17 The pudendal nerve rotransmitter. This system is proposed to \"set continues through the greater sciatic foramen the threshold\" for overall changes, such as, for and enters in a lateral direction, through the instance, in muscle tone under different physio- lesser sciatic foramen, into the ischiorectal logical conditions (sleeping, etc.). The lateral fossa (Alcock's canal). In the posterior part of component of the emotional motor system con- the Alcock's canal, the pudendal nerve gives off sists of discrete areas in the hemispheres and the the inferior rectal nerve; it then branches into the brainstem that are responsible for specific motor perineal nerve and the dorsal nerve of the penis! activities, such as micturition and mating. The clitoris. Although still a controversial matter, it is pathways use spinal premotor interneurons to generally accepted that the pudendal nerve also influence motor neurons in somatic and auto- supplies the urinary and anal sphincter. nomic spinal nuclei, thus, allowing for confluent interactions of various inputs to modify the In contrast, it is mostly agreed that the main motor neuron activity. innervation for the PFM is through direct branches from the sacral plexus (from above) Furthermore, PFM nuclei receive descending rather than predominantly by branches of the corticospinal input from the cerebral cortex. PET pudendal nerve (from below). studies have revealed the activation of the super- omedial precentral gyrus during voluntary PFM Significant variability of normal human neu- contraction, and of the right anterior cingulate roanatomy is probably the source of these contro- gyrus during sustained PFM straining.IS Not sur- versies, originating from anatomical studies of prisingly, PFM contraction can be obtained by the peripheral innervation of the pelvis, which, electrical or magnetic transcranial stimulation of as a rule, are performed in only a small number the motor cortex in men (Fig. 1.2.6).20,21 of cases. Afferent Pathways Descending inputs to PFM motor neurons are manifold, and mostly \"indirect.\" More \"direct\" Because PFM function is intimately connected to connections to Onuf's nucleus are from some pelvic organ function, it is proposed that all nuclei in the brainstem (e.g., raphe or ambigu- sensory information from the pelvic region is rel- ous) and from the paraventricular hypothala- evant for PFM neural control. mus. Positron emission tomography (PET) studies revealed activation of the (right) ventral The sensory neurons are bipolar. Their cell pontine tegmentum (in the brainstem) during bodies are in spinal ganglia. They send a long the holding of urine in human subjects. \" This process to the periphery and a central process finding is consistent with the location of the \"L into the spinal cord, where it terminates segmen- region\" in cats, which is proposed to control PFM tally or, after branching for reflex connections, nuclei. These connections serve the coordinated ascends, in some cases as far as the brainstem.\" inclusion of PFM into \"sacral\" (LUT, anorectal,

28 D.B. Vodusek b The terminals of pudendal nerve afferents in the dorsal horn of the spinal cord are found not c only ipsilaterally but also bilaterally, with ipsilat- eral predominance.\" 50 IlV The proprioceptive afferents form synaptic L... 5ms contacts in the spinal cord and have collaterals (\"primary afferent collaterals\") that run ipsilat- 4.4 8.7 19. 3 erally in the dorsal spinal columns to synapse in the gracillis (dorsal column) nuclei in the brain- II stem. This pathway transmits information about of innocuous sensations from the PFMs. The lateral columns of the spinal cord transmit information concerning pain sensations from perineal skin, as well as sexual sensations. In humans this pathway is situated superficially, just ventral to the equator of the cord, and is probably the spinothalamic tract. \" The spinal pathways, which transmit sensory information from the visceral afferent termina- tions in the spinal cord to more rostral struc- tures, can be found in the dorsal, lateral, and ventral spinal cord columns. Neural Control ofSacral Functions FIGURE 1.2.6. MEPs recorded by concentric needle intheexternal Neural Control ofMicturition urethral sphincter ofa 51-year-old woman. Cortical (a), thoracic (b), and sacral (e) stimulation. Central motor conduction time The LUTis innervated by three sets of peripheral (CMCT) is calculated as cortical-lumbar latency (** = 10.6ms). nerves: parasympathetic nerves (52-54) , which Cauda equina motor conduction time is calculated as lumbar- excite the bladder and relax the urethra (pelvic nerves); sympathetic nerves (Thl l-Lz), which =sacral latency (* 4.3 ms). (Source: Brostrom et al, 2003.) inhibit the bladder body and excite the bladder base and urethra (hypogastric and pelvic nerves); The afferent pathways from the anogenital and somatic nerves (S2-54), which control the region and pelvic region are commonly divided external urethral sphincter and PFM (pudendal into somatic and visceral. Somatic afferents and levator ani nerves). These nerves contain derive from touch, pain, and thermal receptors in afferent (sensory) axons and motor (efferent) skin and mucosa and from proprioceptors in nerve fibers (see Fig. 1.2.7). muscles and tendons. (Proprioceptive afferents especially arise from muscle spindles and Golgi Central nervous system integrative (\"reflex\") tendon organs.) centers responsible for micturition and urinary continence are located in the rostral brainstem in The visceral afferents accompany both para- all species studied, including man, their activity sympathetic and sympathetic efferent fibers, the being modulated by higher centers in the hypo- somatic accompany the pudendal nerves and thalamus and other brain areas, including the direct somatic branches of the sacral plexus. The frontal cortex. Centers in the pons (brainstem) different groups of afferent fibers have different coordinate micturition as such, but centers rostral reflex connections and transmit, at least to some to the pons are responsible for the timing of the extent, different afferent information. start of micturition. The pontine micturition center (PMC) coordinates the activity of motor

1.2. Neural Control ofPelvic Floor Muscles 29 Medial primary motor cortex Medial prefrontal cortee:x..===~~~~~ Hemisphere Brainstem Periaqueductal grey - L region Pontine micturition centre Th oraco lumba l Thoracic sympathet ic Lumbar spinal cord Sacral .'.nucleus _ : >-\" ~~:~::-- : ·······························..····..··..~~~f;S....... nucleus ·····.. Sacral parasympathetic nucleus FIGURE 1.2.7. A schematic presentation of the main integrative and sympathetic (blue) . The most important integrative center areas of lower urinary tract neural control. The three sets of for coordinated storage and emptying of the bladder are in the peripheral nerves are somatic (red), parasympathetic (green), brainstem (black). neurons of the urinary bladder and the urethral overactivity) and an inability to delay voiding at sphincter (both nuclei are located in the sacral inappropriate places and times. spinal cord), receiving afferent input via the peri- aqueductal grey. The central control ofLUT func- Although voluntary micturition is a behavior tion is organized as an on/off switching circuit pattern that starts with the relaxation of striated (or, rather, a set of circuits) that maintains a urethral sphincter and PFM, a voluntary PFM reciprocal relationship between the urinary contraction during voiding can lead to a stop of bladder and urethral outlet. micturition by the \"reverse\" activation of the micturition center (e.g., the \"pattern generator of The PMC has been well studied in experimental voiding\"). Thus, PFM muscle contraction nor- animals, and it has also been demonstrated by mally is necessarily \"accompanied\" by bladder PET in the right dorsomedial pontine tegmentum inhibition. The voluntary \"decision\" is just a in human subjects. Apparently, it is more active on \"push on the button,\" which activates a predeter- the right. \" The PMC sends direct excitatory (glu- mined and integrated motor pattern. taminergic) projections to the parasympathetic detrusor nucleus, and (possibly through the same Neural Control ofContinence pathway) to the GABA-ergic commissural nucleus at the 52-53 spinal level.\" The premotor inter- At rest, continence is assured by a competent neurons from commissural nucleus inhibit the sphincter mechanism, including not only the urethral sphincter. \" The PMC receives descend- striated and smooth muscle sphincter but also ing input from brain areas, and afferent input the PFM and an adequate bladder storage func- from the LUT; the latter it receives indirectly via tion. The kinesiological sphincter EMG record- the periaqueductal grey (in the brainstem).\" ings in normals show continuous activity of Without the PMC and its spinal connections coor- MUPs at rest , increasing with increasing bladder dinated bladder/sphincter activity is not possible; fullness. Reflexes mediating excitatory outflow to thus, patients with such lesions demonstrate the sphincters are organized at the spinal level bladder sphincter discoordination (dyssynergia). (the guarding reflex). The L region in the brain Patients with lesions above the pons do not show has also been called the \"storage center \".\" This detrusor-sphincter dyssynergia; however, they area was active in PET studies of those volunteers suffer from urge incontinence (caused by detrusor who could not void , but could contract their PFM.

30 0.8. Vodusek The L region is thought to exert a continuous ing enteric smooth muscle activity, as well as exciting effect on the Onuf's nucleus and, thus, secretory and absorptive functions of the mucosa. on the striated urinary sphincter during the It has its \"own\" afferents. storage phase; in humans, it is probably part of a complex set of pattern generators for different The colon is innervated by the parasympa- coordinated motor activities, such as breathing, thetic system, the vagus, and the pelvic nerves. coughing, straining, etc. The latter originate from 52-54 cord segments and innervate the descending and sigmoid colon During physical stress (e.g., coughing, and and anorectum. Excitation promotes peristalsis, sneezing), the urethral and anal sphincters are local blood flow, and intestinal secretion. not sufficient to passively withhold the pressures arising in the abdominal cavity and, hence, The medial prefrontal cortex and the anterior within the bladder and lower rectum. Activation cingulate gyrus are thought to regulate the timing of sphincter muscles, as well as the PFMs,is man- and initiation of defecation. datory. (Individuals sensitive to their motor control , for example, are able to feel a tightening Rectal distension causes reflex relaxation of of the PFMs even during a minor stimulus like the smooth internal anal sphincter (the rectoanal taking a deep breath.) This process occurs in inhibitory reflex), allowing the rectal contents to two separate steps by two different activation come into contact with the sensitive anal canal. processes : Simultaneously, the external anal sphincter con- tracts to ensure continence. This physiologic 1. Coughing, sneezing, and deep breathing process is called the \"anal sampling reflex\" and are thought to be generated by individual pattern allows for identification of the rectal contents generators within the brainstem, and, thus, (gas, fluid, or solid). Indeed, it has been demon- coactivation of the PFM is a preset coactivation, strated to occur regularly (up to seven times per and not primarily a \"reflex\" reaction to increased hour) . intraabdominal pressure. Feces stored in the colon is transported past 2. There is a reflex PFM response to increased the rectosigmoid \"physiological sphincter\" into abdominal pressure caused by distension of the normally empty rectum, which can store up muscle spindles within the muscle. This reflex is to 300ml of contents. Rectal distension causes an additional factor in sustaining reflex activa- regular contractions of the rectal wall (effected tion of the PFM. by the intrinsic myenteric plexus) and prompts the desire to defecate. \" In addition, and this is important for any treat- ment program, the PFM can be voluntarily acti- Stool entering the rectum is detected by stretch vated concomitant with the very first awareness receptors in the rectal wall and PFM; their dis- that sneezing or coughing will happen. Such vol- charge leads to the urge to defecate. It starts as untary contraction is part of normal behavior, an intermittent sensation, which becomes more e.g., the ability to control a maximally filled and more constant. Contraction of PFM may bladder or liquid stool-filled rectal ampulla interrupt the process, probably by concomitant during additional physical stress, such as cough- inhibitory influences to the defecatory neural ing. For varying reasons, such coordinated, timed \"pattern generator,\" but also by \"mechanical\" activity is not self-generated by patients, even if insistence on sphincter contraction and the pro- they still have the ability of voluntary pelvic floor pelling of feces back to the sigmoid colon.\" contraction. But they may be able to learn the trick (the Knack procedure). \" PFMare intimately involved in anorectal func- tion. Apart from the \"sensory\" role of PFM and Neural Control ofAnorectal Function the external anal sphincter function, the puborec- talis muscle is thought to maintain the \"anorec- The gastrointestinal tract has its own intrinsic tal\" angle, which facilitates continence, and has innervation, the enteric nervous system, regulat- to be relaxed to allow defecation. Current concepts suggest that defecation requires increased rectal pressure coordinated with the relaxation of the anal sphincters and PFM.Pelvicfloor relaxation allows opening of the

1.2. Neural Control of Pelvic Floor Muscles 31 anorectal angle and perineal descent, facilitating platform\" (contraction of the levator ani and, in fecal expulsion. Puborectalis and external anal the female, the circumvaginal muscles). Climax in sphincter activity during evacuation is generally humans (in both sexes, and in experimental inhibited. However, observations by EMG and animals) elicits rhythmic contractions of the PFM/ defecography suggest that the puborectalis may perineal muscles, which, in the male, dr ives the not always relax during defecation in healthy ejaculate from the urethra (assisted by a coordi- subjects . Puborectalis activity measured by EMG nated reflex bladder neck closure). was unchanged in 9% and increased in 25% of healthy subjects.\" Thus, although \"paradoxical\" Pelvic Floor Muscles in Neurological puborectalis contraction during defecation is (and Idiopathic) Lesions used to diagnose pelvic floor dyssynergia in patients with typical symptoms, this finding may Coordinated detrusor-sphincter activity is re- be related to normal variations also. tained after suprapontine lesions (such as stroke, Parkinson's disease, etc.), indicating the impor- Neural Control ofthe Sexual Response tance of the PMC. However, normal behavioral patterns of sacral function may be altered and Genitals have their own, but in principle similar, voluntary control of the PFM attenuated or lost. peripheral, somatic, parasympathetic, and sym- pathetic innervation from the same spinal cord Coordinated detrusor-sphincter activity is segments by the same sets of nerves as the LUT. lost with lesions between the lower sacral seg- ments and the upper pons (suprasacral infrapon- Erection, seminal emission, ejaculation, and tine lesions), and sphincter inhibition is no longer orgasm are part of the complex mating behavior seen preceding detrusor contractions. On the integrated by the forebrain and hypothalamus. contrary, detrusor contractions are associated The nucleus paragigantocellularis has been with increased sphincter EMG activity. This implicated in the inhibition of climax. This pattern of activity is called detrusor-sphincter nucleus , as well as the periaqueductal grey, dyssynergia.\" Sphincter contraction (or failure receive afferent input from the genitals. of relaxation) during involuntary detrusor con- tractions have been reported in patients with Sexual arousal in men has been associated Parkinson's disease.\" Sphincter behavior in Par- with the activation of the insula and inferior kinsonian patients has been also described as frontal cortex in the right brain hemisphere.\" bradykinetic. The neurogenic uncoordinated sphincter behavior has to be differentiated PFMare activelyinvolved in the sexual response. from \"voluntary\" contractions, which may occur Their activation has been mostly explored in males in poorly compliant patients; the sphincter during ejaculation, where their repetitive activa- contractions of the so-called nonneuropathic- tion during an interval of several seconds is voiding dyssynergia may be a learned abnormal responsible for the expulsion of semen from the behavior.\" urethra, particularly by the bulbospongiosus and the bulbocavernosus muscles.\" Little is known Paradoxical external anal sphincter activation about PFM activity patterns during other parts of during defecation has been described in Parkin- the human sexual response cycle. It is assumed son's disease (anismus\"), Nonrelaxation of the that apart from general changes in muscle tone set puborectalis muscle has been claimed as a major by the emotional motor system, it is the sacral general cause of obstipation, but this is contro- reflex circuit that governs much of the PFM versial. PFM spasm has been described in women activity during the sexual response cycle.\" The as a functional problem in painful intercourse; bulbocavernosus reflex behavior, as found in pre- the entity \"vaginismus\" is, however, controver- vious studies,\" would allow for reflex activation of sial. No EMG changes have been found in one PFMs during genital stimulation. Tonic stimula- study\" and increased basal activity has been tion of the reflex is postulated to hinder venous reported by another. \" Anismus , vaginismus, and outflow from the penis/clitoris, thus, helping erec- pelvic pain derived from \"PFM spasms\" or PFM tion . PFM reflex contraction should conceivably contribute to the achievement of the \"orgasmic

32 D.B. Vodusek overactivity are attractive concepts derived from functionally impaired, with stress incontinence pathophysiological assumptions in various, as and prolapse being a logical consequence. yet unexplained pathological pelvic conditions. The pathological PFM activity in such patients Although muscle weakness may well be a con- has been so far poorly documented, and the con- sequence of childbirth injury, there seem to be ditions remain controversial. further possibilities for deficient PFM function because it is not only the strength of muscle con- Peripheral lesions, either of the motor nuclei in traction that counts. Normal neural control of spinal conus, the nerve roots within cauda equina muscle activity leads to coordinated and timely or the peripheral nerves (the levator ani nerve responses to ensure appropriate muscle function and the pudendal nerve), lead to denervation as required. These muscular behavioral patterns injury of PFM.38 This can be partial or total, and have been studied by kinesiological EMGrecord- results in atrophy. Collateral reinnervation after ing.' Changes in muscular behavior may origi- partial lesions is the rule . Axonal reinnervation nate from minor repairable neuromuscular pelvic after total denervation may not occur for several floor injury.' physiological or anatomical reasons. In healthy nulliparous women, two types of Neuromuscular Injury to the Pelvic behavioral patterns (tonic and phasic) can be Floor Caused by Vaginal Delivery found (Figs. 1.2.8A and 1.2.8B). The tonic pattern consists of a crescendo-decrescendo type of activ- Many studies using different techniques have ity (probably derived from the grouping of slow- demonstrated both neurogenic and structural twitch motor units). The crescendo-decrescendo damage to PFM and sphincter muscles.\" There is pattern may be the expression of constant (tonic) still a role for other lesion mechanisms, such as reflex input parallel to the breathing pattern. muscle ischemia. The implication of all these studies was that the PFMbecomes weak; this can, The phasic pattern, which is probably related indeed, be demonstrated.\" Thus, the sphincter to fast-twitch motor unit activation, is motor unit mechanisms and pelvic organ support become activity seen only during voluntary (phasic) con- traction (e.g., coughing) (Fig. 1.2.1). In respect to these muscle activation patterns, parous women with stress urinary incontinence are subject to several possible changes of these activation patterns.' 111$'.1111111 t+W R.:50 ~V./div. FIGURE 1.2.8. Patterns of H1f l.:50 ~V./div. activation ofpubococ- t cygeus muscles (right Righ t muscle, toptrace; left A Voluntary co ntract io n Lef t muscle, bottom trace) in a normal continent tt t nulliparous woman. (A) Voluntary contraction; (B) B Repetitive cough ing (reflex activat ion) coughing; thetonic pattern from thedetection site on the right, and thephasic pattern ofmuscle activation from theleft. (Source: Reproduced from Deindl et aI., 1993, with permission from Blackwell Publishing Ltd.)

1.2. Neural Control of Pelvic Floor Muscles 33 1\"111111\" . I ; \"l lthUle IlfItI Ul k4U \"\",\"\"1 iIf II I • R t t HW R: 50 ~V/d iv. - - 1 \" HW~lN-1_ _...,..._ _.....l...b. l11f~----- L L: 50 ~V/di v. t t. A i Ii''''m :,\"01:01'1\"011',\":'\",\"' t tB FIGURE 1.2.9. Patterns of activation of pubococcigeus muscles recruitment ofmotor units during acough occurs only on one side (right muscle, top trace; left muscle, bottom trace) in a parous (although both pubococcigeus could be voluntarily activated). stress-incontinent woman (Reproduced from Deindl et aI., 1994, (8)Aparadoxical inhibition offiring ofmotor units occurs during with permission from Blackwell Publishing Ltd.).(A) The expected coughing. 1. Significant reduction of the duration of motor control, which contributes few and poor sensory unit recruitment. data to awareness . Furthermore, its neural control mechanism is fragile because of its relative philo - 2. Unilateral recruitment of reflex response in genetic youth, age, and exposure to trauma and the pubococcygeal muscle (Fig. 1.2.9 A). disease because of its expansiveness of anatomy (from frontal cortex to the \"tail\"). Dysfunctional 3. Inhibition of continuous firing of motor units neural control induced by trauma, disease, or (Fig. 1.2.9 B). purely functional causes may manifest itself by over- or underactivity, and/or by discoordination 4. Delay in PFM activation on coughing. of PFM. Often these disturbances are not \"hard- wired\" into the nervous system, but are only a Although it has not been proven in studies, it problem of neural control \"software\" (which can is reasonable to assume that periods of pain and be \"reprogrammed\"). Therefore, physiotherapy discomfort after childbirth (e.g., perineal tears should, in many patients, provide an appropriate, and episiotomy), and particularly pain related and perhaps the best, treatment. to attempted PFM contraction, could lead to a temporary nona ctivation of the PFM. This could References be the origin of disturbances in behavioral pat- terns, which would need to be readjusted. In 1. Deindl FM, Vodusek DB, Hesse U, et al. Activity combination with a particularly vulnerable pelvic patterns of pubococcygeal muscles in nulliparous floor neural control, which only evolved in its continent women. Br JUrol. 1993;72:46-51. complexity phylogenet ically after the attainment of the upright stance, such a temporary distur- 2. Deindl FM, Vodusek DB, Hesse U, et al. Pelvic bance of neural control after childb irth may floor activity patterns: comparison of nulliparous persist, although the lesion(s) would have fully continent and parous urinary stress incont inent recovered . women. A kinesiological EMG study. Br J Urol. 1994;73:413-417. Conclusion: Neurophysiologic Conceptualization of PFM 3. Kenton K, Brubaker 1. Relationship between Physiotherapy levator ani contraction and motor unit activation PFMs are an axial muscle group under promi- in the urethral sphincter. Am J Obstet Gynecol. nently reflexive and relatively weak voluntary 2002 ;187:403- 4 0 6 . 4. Chantraine A. Examination of the anal and ure- thral sphin cters. In: Desmedt JE, editor. New

34 D.B. Vodusek developments in electromyography and clinical rhizotomy in neurostimulation operations. Neuro- neurophysiology. Volume 2. Basel: Karger, 1973: urol Urodyn. 1993;12:585-598. 421-432. 18. Blok BF, Sturms LM, Holstege G. A PET study on 5. Vodusek DB. Neurophysiological study of sacral cortical and subcortical control of pelvic floor reflexes in man (in Slovene). Institute of Clinical Neurophysiology. Ljubljana: University E. Kardelj musculature in women. I Comp Neurol. 1997;389: in Ljubljana, 1982. 6. Read NW. Functional assessment of the anorec- 535-544 . tum in faecal incontinence. Neurobiology of 19. Holstege G. The emotional motor system in rela- incontinence (Ciba Foundation Symposium 151). Chichester, New York, Brisbane, Toronto, Singa- tion to the supraspinal control of micturition and pore: Iohn Wiley, 1990. mating behavior. Behav Brain Res. 1998;92:103- 7. Borghi F, Di Molfetta L, Garavoglia M, et al. Ques- 109. tions about the uncertain presence of muscle 20. Vodusek DB. Evoked potential testing. Urol Clin spindles in the human external anal sphincter. North Am. 1996;23:427-446. Pan minerva Med. 1991;33:170-172. 21. Brostrom S. Motor evoked potentials from 8. Vodusek DB, Ianko M. The bulbocavernosus the pelvic floor. Neurourol Urodyn. 2003;22: reflex. A single motor neuron study. Brain. 1990; 620-637. 113(Pt 3):813-820. 22. Ueyama T, Mizuno N, Nomura S, et al. Central 9. Sundin T, Petersen I. Cystometry and simultane- distribution of afferent and efferent components ous electromyography from the striated urethral and anal sphincters and from levator ani. Invest of the pudendal nerve in cat. I Comp Neurol. Urol. 1975;13:40-46. 10. Vodusek DB. Electrophysiology. In: Schussler B, 1984;222:38-46. Laycock I, Norton P, et al, editors. Pelvic floor 23. Torrens M, Morrison IF, editors. The physiology re-education: principles and practice. London: of the lower urinary tract. London: Springer- Springer-Verlag, 1994. Verlag, 1987. 11. McCloskey DI. Corollary changes: motor com- 24. Blok BF, van Maarseveen IT, Holstege G. Electrical stimulation of the sacral dorsal gray commis- mands and perception. In: Brookhart 1M, Mount- sure evokes relaxat ion of the external urethral sphincter in the cat. Neurosci Lett. 1998;249:68- castle VB,editors. Handbook of physiology. Section 70. I. The nervous system. Volume 2 (Part 2). Bethesda, 25. Blok BF, Holstege G. The central nervous system MD: American Physiological Society, 1981. control of micturition in cats and humans. Behav 12. Morrison JFB. Reflex control of the lower urinary Brain Res. 1998;92:119-125. tract. In: Torrens M, Morrison JF, editors. The physiology of the lower urinary tract. London: 26. Miller 1M, Ashton-Miller lA, DeLancey 10. Springer-Verlag, 1987. 13. Mannen T, Iwata M, Toyokura Y, Nagashima K. A pelvic muscle precontraction can reduce The Onufs nucleus and the external anal sphinc- cough-related urine loss in selected women ter muscles in amyotrophic lateral sclerosis and with mild SUI. I Am Geriatr Soc. 1998;46:870- Shy-Drager syndrome. Acta Neuropathol (Berl). 874. 1982;58:255-260. 27. Bartolo DC, Macdonald AD. Fecal continence 14. Schroder HD. Anatomical and pathoanatomical and defecation. In: Pemberton IH, Swash M, studies on the spinal efferent systems innervating Henry MM, editors. The pelvic floor. Its function pelvic structures. 1. Organization of spinal nuclei and disorders. London: W. B. Saunders, 2002: in animals. 2. The nucleus X-pelvic motor system 77-83. in man. I Auton Nerv Syst. 1985;14:23-48. 28. Fucini C, Ronchi 0, Elbetti C. Electromyography 15. Barber MD, Bremer RE, Thor KBet al. Innervation of the pelvic floor musculature in the assessment of the female levator ani muscles. Am I Obstet of obstructed defecation symptoms. Dis Colon Gynecol. 2002;187:64-71. Rectum . 2001;44:1168-1175. 16. Bannister LH, ed. Gray's anatomy. The anatomical 29. Stoleru S, Gregoire MC, Gerard D, et al. Neuro- basis of medic ine and surgery. 38th edition. New anatomical correlates of visually evoked sexual York, London : Churchill Livingstone, 1995. arousal in human males. Arch Sex Behav. 1999; 17. Marani E, Pijl ME, Kraan MC et al. Inter- 28:1 -21. connections of the upper ventral rami of the 30. Petersen I, Franksson C, Danielson CO. Electro- human sacral plexus : a reappraisal for dorsal myographic study of the muscles of the pelvic floor and urethra in normal females. Acta Obstet Gynecol Scand. 1955;34:273-285. 31. Vodusek DB. Sacral reflexes. In: Pemberton IH, Swash M, Henry MM, eds. Pelvic floor. Its func- tions and disorders. London: Saunders, 2002.

1.2. Neural Control of Pelvic Floor Muscles 3S 32. Blaivas JG, Sinha HP, Zayed AA, Labib KB. exposure to emotion-inducing film ex-cerpts in Detrusor-external sphincter dyssynergia: a women with and without vaginismus. Int Urogy- detailed eiectromyographic study. J Uro!. 1981;125: necol J Pelvic Floor Dysfunct. 2001iI2:328-331. 545-548. 37. Graziottin A, Bottanelli M, Bertolasi 1. Vaginis- mus: a clinical and neurophysiological study. Uro- 33. Pavlakis AJ, Siroky MB, Goldstein I, Krane RJ. dinamica.2004;14:117-121. Neurourologic findings in Parkinson's disease. 38. Podnar S, Oblak C, Vodusek DB. Sexual function J Uro!. 1983iI29:80-83. in men with cauda equina lesions : a clinical and electromyographic study. J Neurol Neurosurg Psy- 34. Rudy DC, Woodside JR. Non-neurogenic neuro- chiatry. 2002;73:715-720. genic bladder: The relationship between intra- 39. Vodusek DB. The role of electrophysiology in the vesical pressure and the external sphincter evaluation of incontinence and prolapse. Curr electromyogram. Neurourol Urodyn . 1991;10:169. Opin Obstet Gyneco!. 2002iI4:509-514. 40. Verelst M,Leivseth G.Are fatigue and disturbances 35. Mathers SE, Kempster PA, Law PJ, et a!. Anal in pre-programmed activity of pelvic floor muscles sphincter dysfunction in Parkinson's disease. associated with female stress urinary inconti- Arch Neuro!. 1989i46:1061-1064. nence? Neurourol Urodyn. 2004;23:143-147. 36. van der Velde J, Laan E, Everaerd W. Vaginismus , a component of a general defensive reaction. An investigation of pelvic floor muscle activity during

1.3 The Effects of Pregnancy and Childbirth on the Pelvic Floor Kaven Baessler and Bernhard Schussler Key Messages • Antepartum pelvic floor exercises led to a decline of postpartum stress urinary incontinence. • Connective tissue remodeling before delivery and intrapartum trauma play major roles in Introduction pelvic floor dysfunction after childbirth. For many years, vaginal delivery has been consid- • Frequency, stress incontinence, and, to a ered a principle causal factor in the development lesser extent, overactive bladder increase in the of incontinence and pelvic organ prolapse.P :' course of pregnancy and show a decline after Recent large , community-based epidemiological delivery. studies have revealed that pregnancy itself, with its associated hormonal, connective tissue, and • Stress incontinence occurs in up to 85% of physical changes, plays a major role, with vaginal women during pregnancy, in 22% postpartum, and instr umental delivery only further increas- and in 4-19% de novo after childbirth. ing the risk of pelvic floor dysfunction.v\" Elective cesarean section is commonly believed to pre - • Stage II pelvic organ prolapse, especially ante- serve pelvic floor function. Although it might sig- rior vaginal wall prolapse, is not uncommon nificantly reduce the risk of pelvic organ prolapse during pregnancy. and anal sphincter defects, it does not necessarily protect against urinary and anal incontinence in • After vaginal delivery, the position of the the long term/ \" Muscular, nerve, and connective perineum and bladder neck are lower and the tissue damage has been demonstrated in up to pelvic floor contraction strength is reduced. 80% of women after vaginal deliveries/ but these changes do not automatically result in pelvic floor • Reinnervation as a sign of denervation is pre- dysfunction symptoms. Epidemiological studies sent in 80% of women postpartum, but also have also emphasized the effect of promoting progresses over time and with ageing . factors; inevitable influences like ageing and genetic predisposition v' \" and often avoidable risk • Obesity and age are major risk factors for the factors like obesity, constipation, and hormone development of pelvic floor dysfunction. replacement therapy. Recent research has ques- tioned the value of previously routine interven- • Risks factors for anal sphincter laceration tions like midline and mediolateral episiotomy, include first delivery, occipitoposterior pre- but has also investigated the effects of forceps and sentation, a prolonged second stage of labor, vacuum, which are used for instrumental deliver- forceps delivery, higher birth weight , and ies, on the pelvic floor,\" maternal age greater than 35 years. • Routine mediolateral and midline episiotomy do not prevent pelvic floor trauma or protect the baby, and they are obsolete . • Cesarean section is only partially protective and might reduce, but not totally prevent, pelvic floor dysfunction. 36

1.3. The Effects of Pregnancy and Childbirth on thePelvic Floor 37 There are two main events before and during stretched to greater lengths during pregnancy, childbirth that concern the whole body, and the but were also much weaker. In some women, pelvic floor in particular; hormonal preparation these changes may be irreversible, or further for childbirth, which allows dense connective stretching beyond physiological limits (e.g. tissue to soften, and mechanical trauma during during vaginal delivery) may result in permanent vaginal delivery. This chapter presents an update dysfunction. of our current knowledge on the effects of preg- nanc y and childbirth on the pelvic floor and Mechanical Trauma pelvic floor symptoms. The influence of episiot- omy, instru mental delivery, and positioning There is little doubt that vaginal delivery consti- during vaginal birth are described and, subse- tutes a traumatic event to the pelvic floor, but we quently, emerging possible strategies for pelvic are not certain about the mechanisms that lead floor protection are discussed. Many studies on to complete restitution or result in anatomical or this topic have underutilized instruments such as functional changes. Mechanical damage to the quality of life assessments, and the lack of con- pelvic floor musculature, connective tissue, and sistency in terminology and definition of out- nerve supply usually occurs during the second comes prevents comparison between studies. stage of labor when the fetal head distends and stretches the pelvic floor (Fig. 1.3.1; see also Hormones: Changes and Impact dynamic 3D image on DVD). Lien et al. have developed a pelvic model from MRI studies to Hormonal alterations are physiological and examine behavior and interaction of the baby's essential to prepare the body and to adjust the head and the pelvic floor muscle. The most medial musculature and connective tissue for vaginal part of the puboco ccygeus muscle is the part of birth. It seems reasonable to assume that some of the pelvic floor that undergoes the largest stretch- these transformations might not have reversed in ing, i.e. up to 3.26 times its original length,\" women with considerable postpartum anatomi- cal and functional pelvic floor changes. This is FIGURE 1.3.1. Pelvicfloor distension during vaginal delivery. Note particularly true in the case of evident damage the stretching of the puborectalis and pubococcygeus muscle after cesarean delivery, when mechanical trauma and theseparation ofthe perineal membrane. According to Lien to the pelvic floor was avoided. et al,\" the pubococcygeus muscle has the greatest rest/stretch ratio during vaginal delivery; itstretches to3.26 times itsoriginal Diminishing pelvic floor function during preg- length. (Source:Modified from Schussler B, Anthuber C, Warrell D. nancy is at least partly related to the effects of the The pelvic floor before and after delivery. In:Schussler B, Laycock high progesterone levels during pregnancy. Pro- J, Norton P,Stanton S, editors. Pelvic floor re-education. Principles gesterone is known to reduce the tonus in ureters, and Practice. Springer-Verlag London Ltd; 1994:871994:105.) bladder, and urethra because of its smooth muscle-relaxing and estrogen-antagonizing ef- fects.\" Relaxin, which is a peptide hormone similar to insulin, increases markedly during pregnancy. It modifies the connective tissue and has a collagenolytic effect to allow for appropri- ate stretching during vaginal birth in guinea pigs.\" This hormone also seems to be responsible for pelvic and symphyseal pain. \" There might be many hormones involved in conne ctive tissue remodeling and cervical ripening, e.g. increasing joint mobility in pregnancy is well known. \" As a likely result of connective tissue remodeling in preparation for birth, Landon and colleagues\" found that the connective tissue of the rectus sheath fascia and the obturator fascia could be

38 K. Baessler and B. Schiissler Apart from the mechanical trauma - direct pelvic floor changes. Stress incontinence during muscle rupture or, more commonly, stretching - pregnancyis reported by up to 85%ofwomen,17,18,19 there might also be biochemical damage to the soft tissue, especially during long second stages with an increasing incidence from 10% at 12 when the fetal head is compressing the pelvic weeks to 23% at 24 weeks and 26% at 36 weeks of floor. Currently, it is not possible to determine gestation in one study,\" Urgency symptoms are exactly whether pelvic floor symptoms are attrib- found in 23% of women, but urge incontinence is utable to impa irment caused by hormonal modi- not as common in 8% (Fig. 1.3.2).18 Voiding diffi- fication (and lack of reversal) or mechanical culties can also occur during pregnancy, with forces or a combination of both. 43% of women in one study complaining of a poor stream and 37% of incomplete bladder emptying.\" The Pelvic Floor During Pregnancy Findings During Pregnancy: Pelvic Organ Prolapse and Urodynamics Hormonal and mechanical changes, along with the growing uterus displacing and distorting the Examination bladder, may contribute to pelvic floor dysfunc- tion during pregnancy. The physiological weight During pregnancy, the blood flow to the pelvic gain during pregnancy might also playa role. An organs and the pelvic floor increases, connective increased body mass index correlates with the tissue becomes more elastic, and there is hyper- intraabdominal pressure during urodynarnics\" trophy of smooth muscle and hyperplasia of and has repeatedly been shown to be an indepen- mucous membranes.\" Three recent studies have dent risk factor for urinary incontinence later in drawn attention to the occurrence of clinically life. significant pelvic organ prolapse during preg- nancy in nulliparous women. All three studies Symptoms employed the validated quantification of pelvic organ prolapse of the International Continence Increased daytime and nighttime urinary fre- Society. O'Boyle et al. used a case-control study quency is a very common symptom in pregnant of21 nulliparous women at 14-39 weeks of gesta- women.\":\" Although the increase in urinary fre- tion and found stage 2 pelvic organ prolapse quency might predominantly result from the (leading edge of prolapse +/- 1ern of the hymenal increase in glomerular filtration rate, stress remnants) in 48%, whereas none of the 21 age- incontinence symptoms are clearly a sign of and race-matched nonpregnant controls demon- strated stage 2 prolapse .\" Another study assessed 35 A. / <, 30 -+- Stress incontinence 25 <, _ Urge incontinence 20 <, --.- Anal incontinence <; •15 FIGURE 1.3.2. Stress and urge inconti- ~ ................. nence and anal incontinence during preg- 10 nancy and after delivery in primiparous 5 women.17.18.20 --- •o

1.3. The Effects of Pregnancy and Childbirth onthePelvic Floor 39 pelvic organ prolapse at 36 weeks of gestation in Childbirth and Pelvic Floor Function 94 women.\" It revealed stage 2 prolapse in 26%.24 Cross-sectional comparisons of pelvic organ pro- Hormonal changes will affect all pregnant lapse in the first, second, and third trimester also women; yet, the extent may vary widely. If a confirmed that there is more stage 2 pelvic organ woman undergoes cesarean section, the extent prolapse in the third trimester (18/52; 35%).25The might depend on the timing. Premature delivery most frequent site of prolapse was the anterior or elective or emergency cesarean section after vaginal wall in all of these studies. Interestingly, labor has already progressed might have differ- the latter study also demonstrated a clinically ent effects because of the different hormonal significant increase in perineal body length of changes and trauma. This part of the chapter almost 1em from the first to the third trimester. describes the immediate effects of childbirth on Genital hiatus and total vaginal length increased the pelvic floor anatomy and function and the by approximately 5 mm.\" The lengthening of the impact of intrapartum interventions, and it perineal body during pregnancy is an intriguing attempts to place the findings into the long-term finding, given that a short perineum «4cm picture drawn by the new epidemiological during the first stage of labor) was associated studies. with higher episiotomy and vaginal tear rates, although the overall number of episiotomy in Findings on Clinical Examination After nulliparous women in that study was rather high Vaginal Delivery at 76%.26 Imaging The position of the perineum is lower after vaginal delivery (Fig. 1.3.3, A and B).32 Employing Many studies have compared bladder neck mobil- the International Continence Society (ICS) pelvic ity before and after delivery, but, unfortunately, organ prolapse standardization, Sze et al. pro- there is a paucity of prospective data on changes spectively studied nulliparous women and found that occur during pregnancy. However, compara- that postpartum 52% had stage 2 prolapse, 37% tive studies demonstrated that the urethrovesical had developed a new prolapse, and 15% revealed angle at rest is increasing during pregnancy\" and a more severe prolapse compared to antenatal is significantly wider compared to nonpregnant examinations.\" Pelvic floor muscle contraction controls, \" and that the bladder neck shows an strength is reduced after vaginal delivery, which increased \"backward displacement\" antenatally has been demonstrated with several investigation compared with a nonpregnant control group.\" techniques used: vaginal cones,\" standardized This correlates well with the aforementioned physical examination assessment of pelvic floor increase in anterior vaginal wall prolapse during muscle strength,\" intravaginal squeeze pressure pregnancy. measurement.s\":\" and perineal ultrasound.\" However, there seems to be some recovery of the Urodynamic Studies lowered perineal position\" and pelvic floor con- traction strengtlr' ' :\" 6 weeks to 3 months post- Urodynamic studies during pregnancy have been partum. The exact mechanisms of recovery or rather inconsistent in their findings. The urethral deterioration remain unknown. closure pressure and the functional urethral length were shown to increase during the course Neurophysiology of pregnancy according to one study,\" whereas they remained unchanged in another.\" Com- Intact innervation of the levator ani muscle, anal, pared with nulliparous nongravid controls, the and urethral sphincters is critical to normal maximum urethral closure was lower during pelvic function. Techniques to measure the com- pregnancy,\" petency of the nerve supply are often invasive (needle electromyography [EMG]) or not very

40 K. Baessler and B. Schussler Rectum Perineal body Descent 13 mm ~==::!~~ Perineal position on straining Descent 17 mm on stra in ing A B FIGURE 1.3.3. Position ofthebladder neck and perineum at rest and on straining during pregnancy in nulliparas (A) and after vaginal delivery (B). While the positions at rest remain unchanged postpartum, thedescent ofthe bladder neck and the perineum during straining increases significantly.J2,J5 specific and prone to disturbances (surface EMG) thirds of the women with an abnormally pro- or the exact implications are not clear (pudendal longed PNTML after delivery had normal nerve terminal motor latency [PNTML]). measurements six months later.\" Single-fiber EMG, as well as concentric-needle Findings onUrodynamics EMG, can identify partial denervation by signs of reinnervation, such as increased fiber density. Prospective urodynamics studies performed Prospective EMG studies performed before and during pregnancy and six to nine weeks postpar- after childbirth substantiated the evidence of tum revealed a notable decrease in urethral childbirth-induced pelvic floor denervation, closure pressure\" and urethral length'S\":\" after detecting increased fiber density after vaginal vaginal delivery. Women with persisting urinary delivery/:\" There is evidence of reinnervation in incontinence after childbirth were found to have 80% of women after vaginal delivery.' Snooks a shorter functional urethral length and a lower et a1.37 investigated 14 multiparous women from urethral closure pressure compared with conti- their previous studiea\":\" after five years and nent women.\" demonstrated that pelvic floor denervation pro- gressed, indicating that age is a contributory Findings on Perineal Ultrasound factor,\" Similarly, progressive denervation with time up to 15 years postpartum was found in Bladder neck mobility increases and the bladder another prospective study, corroborating the neck position is lower after vaginal delivery, as ageing factor.?\" imaged by perineal ultrasound (Fig. 1.3.3, A and B).19,35,36 Women with postpartum stress inconti- Prolongation of the PNTML is thought to be a nence were found to have greater bladder neck result of pudendal nerve damage during vaginal mobility during straining before delivery com- delivery. Significantly prolonged mean PNTML's pared with continent women.\" It remains unclear, have been found in women two to three days after however, whether the lower observed bladder vaginal delivery, compared to a multiparous\" neck position is caused by impaired connective and a nulliparous control group.\" At follow-up tissue structures, by reduced levator ani muscle five years later, prolongation of PNTML per- tone, or by both. Specific pelvic floor muscle sisted.\" Two prospective analyses demonstrated trauma can be depicted with MRI and 3D ultra- a prolongation of the PNTML antenatally to six sound (see Imaging Chapter 2.4). to eight weeks after vaginal delivery, particularly after the first delivery.\":\" But, again, many of these changes seem to be temporary, as two-