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Pathophysiology of Urinary Incontinence, Faecal Incontinence and Pelvic Organ Prolapse

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Pathophysiology of Urinary Incontinence, Faecal Incontinence and Pelvic Organ Prolapse Committee 4 Pathophysiology of Urinary Incontinence, Faecal Incontinence and Pelvic Organ Prolapse Chairman H. KOELBL (Germany) V. NITTI (USA) Members K. BAESSLER (Germany), S. SALVATORE (Italy), A. SULTAN (U.K), O. YAMAGUCHI (JApan) 255 CONTENTS PREFACE E. FAECAL INCONTINENCE: GASTROENTEROLOGICAL PERSPECTIVE A. THE OVERACTIVE BLADDER F. CHILDBIRTH AND FAECAL B. PREGNANCY, CHILDBIRTH INCONTINENCE AND THE PELVIC FLOOR G . PATHOPHYSIOLOGY OF INCONTINENCE IN MEN C. PATHOPHYSIOLOGY OF STRESS INCONTINENCE IN H. CAUSES OF TRANSIENT WOMEN: URETHRAL INCONTINENCE IN OLDER STRUCTURE, ADULTS SUPPORT AND FUNCTION D. PELVIC ORGAN PROLAPSE REFERENCES LIST OF ABBREVIATIONS ACS American College of Surgeons LUTS Lower Urinary Tract Symptoms ANS Autonomic Nervous System MRI Magnetic Resonance Imaging ACh Acetylcholine MS Multiple Sclerosis AChE Acetylcholinesterase NO Nitric Oxide ASR Anal Sphincter Rupture NOS Nitric Oxide Synthase ATP Adenosine Triphosphate NGF Nerve Growth Factor BPH Benign Prostatic Hyperplasia OAB Overactive Bladder BPO Benign Prostatic Obstruction PMC Pontine Micturition Center PFD Pelvic Floor Dysfunction CNS Central Nervous System POP Pelvic Organ Prolapse CI Confidence Interval POPQ Pelvic Organ Prolapse Quantitation cAMP Cyclic Adenosine Monophosphate PNTML Pudendal Nerve Motor Terminal Motor DO Detrusor Overactivity Latency DM Diabetes Mellitus RRP Radical Retropubic Prostatectomy DSD Detrusor Sphincter Dyssynergia RCOG Royal College of Obstetricians and EMG Electromyography Gynaecologists EAS External Anal Sphincter SSRI Selective Serotonin Re-uptake Inhibitor IBD Inflammatory Bowel Disease STRESS URINARY INCONTINENCE IBS Irritable Bowel Syndrome Stress Urinary Incontinence IAS Internal Anal Sphincter TURP Transurethral Prostatectomy ICI International Consultation on TUIP Transurethral Incision of the Prostate Incontinence TTX Tetrodotoxin IPSS International Prostate Symptom Score VLPP Valsalva Leak Point Pressure ISD Intrinsic Sphincter Deficiency USI Urodynamic Stress Incontinence 256 Pathophysiology of Urinary Incontinence, Faecal Incontinence and Pelvic Organ Prolapse H. KOELBL, V. NITTI, K. BAESSLER, S. SALVATORE, A. SULTAN, O. YAMAGUCHI neural stimulation of the striated sphincter appear, PREFACE and the limits of vaginal suspensory operations for correction of urethral dysfunction are reported, For this fourth International Consultation on considerations of pathophysiology have shifted from Incontinence, the Committee on Pathophysiology is the 50 year old paradigm regarding urethral mobility organized to consider causes of pelvic prolapse and associated with vaginal prolapse in the genesis of faecal, as well as urinary incontinence. For any woman, incontinence. However, these newer directions should childbirth and pregnancy contribute to the development be considered against the background of half a century of urinary as well as faecal incontinence; therefore of observation and practical clinical experience. We these two conditions have been naturally integrated therefore continue to recommend a balanced into a single chapter. Special problems of the elderly approach. have also been included for this ICI. We have also In the area of men’s incontinence, the greatest concern been asked to consider pathophysiological remains the problem of sphincter injury following mechanisms underlying pelvic organ prolapse. These radical pelvic surgery and brachytherapy. While many three areas urinary incontinence, pelvic organ prolapse thousands of procedures are performed annually, our and faecal incontinence, are closely interconnected knowledge about sphincter anatomy and function has by virtue of similar location within the body. In the progressed little. Instead, empirical methods of case of women, childbirth and pregnancy may treatment and hopefully prevention have been contribute to one or all of these conditions. Yet there advanced to treat affected individuals, and insofar as are also neurological factors, and gender specific prosthetic implants remain an effective method of factors which must be considered in the evaluation of treatment, enthusiasm for further basic research into any given patient. Thus, we have tried to provide a male sphincter function remains limited. In contrast to balanced overview of the subject, keeping in mind this kind of sphincter injury, the causes of incontinence both the common and the distinct qualities of the associated with bladder outlet obstruction and prostatic various conditions, while organizing them in a logical, enlargement have been well characterized, and little narrative manner that make any one section of the new knowledge has appeared in recent years. Finally, chapter easy to read. with respect to faecal incontinence and pelvic organ In the area of women’s stress incontinence, intrinsic prolapse, two areas for this Committee’s concern, the urethral function continues to receive increased sections addressing them may appear to provide attention. As newer pharmacological agents to provide some overlap and possible redundancy. 257 also have dual excitatory and inhibitory influences on reflex bladder activity [11]. It has been demonstrated A. THE OVERACTIVE BLADDER that in the rat cerebral infarction model, bladder overactivity is mediated by NMDA glutamatergic and D2 dopaminergic excitatory mechanisms [8], suggesting that cerebral infarction may alter a balance I. INTRODUCTION between the facilitatory and inhibitory mechanism that results in up regulation of an excitatory pathway and The most common problem with urine storage arises downregulation of a tonic inhibitory pathway. Similarly, when the bladder fails to remain relaxed until an neuropharmacological studies in a monkey model for appropriate time for micturition. The symptom Parkinson’s disease have shown that detrusor syndrome is called “overactive bladder”(OAB), which overactivity may result from a loss of dopaminergic refers to the symptoms of urgency, with or without inhibition mediated by D1 receptors [4, 7]. urge incontinence, usually with frequency and nocturia [1]. According to the ICS terminology of 2002 [1], OAB symptoms are suggestive, but not diagnostic, of urodynamically demonstrable detrusor overactivity (involuntary detrusor contraction) during the filling phase which may be spontaneous or provoked. This may be further characterized as neurogenic when there is a relevant neurological condition. Common neurogenic causes include stroke, Parkinson’s disease, multiple sclerosis and spinal injury. Non- neurogenic etiologies may be related to outflow obstruction, aging estrogen deficiency, female anatomical incontinence, but most cases are idiopathic. This section focuses on pathophysiology of the overactive bladder and reviews studies that have provided insight into the mechanisms underlying bladder overactivity and OAB symptoms. II. NEUROGENIC DETRUSOR OVERACTIVITY Figure 1: Suprapontine lesions causing detrusor overactivity 1. SUPRAPONTINE LESIONS (Figure1) 2. SPINAL CORD LESIONS (Figure 2) It is generally accepted that suprapontine lesions such as cerebrovascular disease and Parkinson’s disease A spinal cord lesion above the lumbosacral level produce detrusor overactivity. The patient with a eliminates voluntary and supraspinal control of suprapontine lesion loses voluntary inhibition of micturition, leading to bladder overactivity mediated micturition, which corresponds to uninhibited overactive by spinal reflex pathways [4, 12]. Disruption below bladder according to a classification by Fall et al [2, the level of the pons leads to unsustained and 3]. uncoordinated detrusor contractions often associated with uncoordinated sphincter overactivity (detrusor- Brain transaction studies in animals with an intact sphincter dyssynergia, DSD). Impairment or loss of neuroaxis showed that suprapontine areas generally bladder sensation is a typical feature. exert a tonic inhibitory influence on the pontine micturition center (PMC) [4, 5]. In humans, the cerebral Electrophysiologic studies of the effect of capsaicin on cortex (medial frontal lobes) and the basal ganglia voiding reflexes have shown that the afferent limb of are thought to suppress the micturition reflex. Thus, the micturition reflex in chronic spinal cats, consists damage to the brain induces bladder overactivity by of unmyelinated C-fibre afferents, whereas in normal reducing suprapontine inhibition. cats it consists of myelinated A-delta afferents [4, 13, The mechanism of overactive bladder induced by 14]. Since C-fibre bladder afferents in the cat do not cerebral infarction or Parkinson’s disease has been usually respond to bladder distension [15], a further studied using animal models [6-8]. In the central considerable reorganization of reflex connections nervous system, a glutamatergic pathway is known takes place in the spinal cord following the interruption to play a role in both excitatory and inhibitory regulation of descending pathways from the brain. In humans with of micturition [6, 9, 10]. Central dopaminergic pathways spinal cord lesions, neurogenic detrusor overactivity 258 is likely to be mediated by capsaicin-sensitive C-fibre III. NON-NEUROGENIC DETRUSOR afferents. Clinical experience with capsaicin supports the role of these C-fibre afferents in the pathophy- OVERACTIVITY siology of neurogenic bladder overactivity. Capsaicin has been used for the treatment of neurogenic bladder 1. OUTFLOW OBSTRUCTION (Figure 3) overactivity in patients with spinal cord injury or multiple Detrusor overactivity associated with outflow sclerosis.
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