Evaluation of Urinary Incontinence (original) (raw)

Neural control of the lower urinary tract: Peripheral and spinal mechanisms

Neurourology and Urodynamics, 2010

This review deals with individual components regulating the neural control of the urinary bladder. This article will focus on factors and processes involved in the two modes of operation of the bladder: storage and elimination. Topics included in this review include: (1) The urothelium and its roles in sensor and transducer functions including interactions with other cell types within the bladder wall ("sensory web"), (2) The location and properties of bladder afferents including factors involved in regulating afferent sensitization, (3) The neural control of the pelvic floor muscle and pharmacology of urethral and anal sphincters (focusing on monoamine pathways), (4) Efferent pathways to the urinary bladder, and (5) Abnormalities in bladder function including mechanisms underlying comorbid disorders associated with bladder pain syndrome and incontinence.

Anatomy and Neurophysiology of the Lower Urinary Tract and Pelvic Floor

Urodynamics, Neurourology and Pelvic Floor Dysfunctions, 2018

The urinary tract undergoes a very dynamic development during foetal life. Emerging from the metanephros, the human kidney begins to produce urine at 10-12 weeks of gestation [1, 2]. At this time the bladder is a cylindrical tube of cuboidal cells in a single layer. During the second trimester, 4-5 cell layers develop, forming a low compliant 'bladder' at the 21st week of gestation [3-5]. The foetal bladder handles a relatively large amount of fluid, draining to the amniotic cavity with a subsequent oral reuptake by the foetus. The salt and water homeostasis, however, is cleared by the placenta and eventually by the mother's kidneys [6]. Any deviation from this cycle may lead to a more or less pathological consequence for the foetus. In the beginning the lower urinary tract is a conduit with coordinated peristalsis propulsing the urine through the urethra, as is the case with the upper urinary tract. After the formation of the external sphincter, the lower urinary tract develops graduate filling and emptying, and the bladder wall properties change. From being a coordinated peristaltic conduit, the bladder becomes an organ with chaotic micromotions in the bladder wall.

Bladder outlet physiology in the context of lower urinary tract dysfunction

Neurourology and Urodynamics, 2011

Physiological function of the bladder outlet is complex and symptomatic consequences can result from outlet dysfunction. Within the outlet, smooth, and skeletal muscles constitute the contractile apparatus, but additional cell types include interstitial cells and neuroendocrine cells, and various transmitters are present in the innervation, raising the possibility of unrecognized functional subtleties. Key outlet functions are; maintained closure for urine storage, increased closure (guarding) during exertion, sustained opening for voiding, transient opening for territorial marking in animals and orthograde male ejaculation. These are coordinated by several spinal and higher CNS centers, with overlap of the somatic, sympathetic and parasympathetic nervous systems. During voiding, urethral afferents may be important in maintaining detrusor contraction until completion of bladder emptying. Some of the bladder outlet afferents may be shared with the anal sphincter. Dysfunction of the outlet leads to conditions such as retrograde ejaculation, Fowler's syndrome, and detrusor sphincter dyssynergia. Urethral relaxation during urine storage may lead to urinary urgency, which may be misleadingly labeled as overactive bladder. Research priorities are numerous, including; peripheral cellular integrative physiology, interactions with other pelvic organs, interconnectivity of the CNS centers at all levels of the neuraxis, and standardized animal models of outlet functions such as reflex-driven voiding.

The neural control of micturition

Nature Reviews Neuroscience, 2008

Micturition, or urination, occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. The neural circuitry that controls this process is complex and highly distributed: it involves pathways at many levels of the brain, the spinal cord and the peripheral nervous system and is mediated by multiple neurotransmitters. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary or reflex micturition, leading to urinary incontinence. This is a major health problem, especially in those with neurological impairment. Here we review the neural control of micturition and how disruption of this control leads to abnormal storage and release of urine.