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Urinary incontinence is a condition with multi-factorial aetiology and a complex pathophysiological basis. However, the underlying principles are relatively simple. In this article we consider these pathophysiological elements in separate sections to emphasise how they interact to effect a change in lower urinary tract pressures during different phases of the micturition cycle. The interstitial cells have a key sensory role in the bladder, with much research currently taking place to investigate their exact function. Neural pathways, by comparison, are relatively well established and interactions between the pontine micturition centre (PMC) in the brain stem and the sacral micturition centre (SMC) in the sacral spinal cord, with voluntary control from higher centres, provide neurological control of the lower urinary tract. Depending on the level of a neurological deficit or injury, certain recognizable patterns of bladder dysfunction can be identified. Mechanical factors – the pelvic floor, striated sphincter muscles and smooth muscles of the bladder and urethra – also play a major role in maintaining normal continence. Dysfunction of any of these elements can cause, to varying degrees, a loss of urethral pressure, a rise in bladder pressure, or both. This imbalance results in incontinence. An understanding of this principle, and the pathophysiological mechanisms behind it, will help guide investigation and treatment choices to best manage patients with this unfortunate condition. |
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