Morphology and neuropathology of the pelvic floor in patients with stress incontinence.
Urinary incontinence imposes a considerable workload on urological and gynecological practice. Many treatments exist, but recurrent stress incontinence remains a significant problem and the reasons remain unclear. Pathological and electrophysiological studies have shown that significant pelvic nerve damage and consequent denervation and reinnervation are associated with stress incontinence, and furthermore there are collagenous changes in the pelvic floor which are related to childbirth, endogenous hormone changes and the effects of increasing age. These changes include increased nerve fiber density and pudendal nerve terminal motor latency, hypertrophy of fiber types 1 and 2, type 1 fiber predominance and fiber type grouping. Connective tissue changes involve a reduction in hydroxyproline excretion, increased cross-linking and increased muscle collagen. It is only through a better understanding of the anatomy and pathophysiology of the pelvic floor that we will be able to improve outcome in women with stress incontinence and identify patients that may not be appropriate for surgical therapy. This paper reviews recent advances in the understanding of the etiology of stress incontinence.
Morley
R
R
Department of Urology, Southampton University Hospital, UK.
Cumming
J
J
Weller
R
R
D000367:Age Factors; D001284:Atrophy; D003094:Collagen / Q000096:biosynthesis; D005260:Female; D006801:Humans; D006984:Hypertrophy; D018482:Muscle, Skeletal / Q000473:pathology*; D009412:Nerve Fibers / Q000473:pathology; D017773:Pelvic Floor / Q000294:innervation* / Q000473:pathology / Q000503:physiopathology; D011247:Pregnancy; D014550:Urinary Incontinence, Stress / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology
D003094:Collagen